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| 1 | Ferroptosis is an autophagic cell death process显示文摘Ferroptosis 是调整坏死的一种铁依赖者形式。它在各种各样的人的疾病被含有,包括 ischemic 机关损坏和癌症。这里,我们报导 autophagy 的关键角色,特别地细胞的铁存储蛋白质(作为 ferritinophagy 知道的一个过程) 的 autophagic 降级,在 ferroptosis。用 RNAi,屏蔽结合了随后的基因分析,我们作为 ferroptosis 的积极管理者识别了多重 autophagy 相关的基因。Ferroptosis 正式就职导致了 autophagy 激活和 ferritin 和 ferritinophagy 货物受体 NCOA4 的作为结果的降级。一致地,由 autophagy 的阻塞的 ferritinophagy 的抑制或废除的 NCOA4 击倒联系 ferroptosis 的细胞的易变的铁的累积和反应的氧种类,以及最终的 ferroptotic 细胞死亡。因此, ferroptosis 是一个 autophagic 房间死亡过程,并且调停 NCOA4 的 ferritinophagy 由控制细胞的铁动态平衡支持 ferroptosis。 | Minghui Gao Prashant Monian Qiuhui Pan Wei Zhang Jenny Xiang Xuejun Jiang | 2016 | Cell Research2016，26，9： | 138 |
| 2 | Autophagy and inflammation in ischemic stroke显示文摘Appropriate autophagy has protective effects on ischemic nerve tissue,while excessive autophagy may cause cell death.The inflammatory response plays an important role in the survival of nerve cells and the recovery of neural tissue after ischemia.Many studies have found an interaction between autophagy and inflammation in the pathogenesis of ischemic stroke.This study outlines recent advances regarding the role of autophagy in the post-stroke inflammatory response as follows.(1)Autophagy inhibits inflammatory responses caused by ischemic stimulation through mTOR,the AMPK pathway,and inhibition of inflammasome activation.(2)Activation of inflammation triggers the formation of autophagosomes,and the upregulation of autophagy levels is marked by a significant increase in the autophagy-forming markers LC3-II and Beclin-1.Lipopolysaccharide stimulates microglia and inhibits ULK1 activity by direct phosphorylation of p38 MAPK,reducing the flux and autophagy level,thereby inducing inflammatory activity.(3)By blocking the activation of autophagy,the activation of inflammasomes can alleviate cerebral ischemic injury.Autophagy can also regulate the phenotypic alternation of microglia through the nuclear factor-κB pathway,which is beneficial to the recovery of neural tissue after ischemia.Studies have shown that some drugs such as resveratrol can exert neuroprotective effects by regulating the autophagy-inflammatory pathway.These studies suggest that the autophagy-inflammatory pathway may provide a new direction for the treatment of ischemic stroke. | Yun Mo Yin-Yi Sun Kang-Yong Liu | 2020 | Neural Regeneration Research2020，15，8： | 90 |
| 3 | Antitumor effect of matrine in human hepatoma G2 cells by inducing apoptosis and autophagy显示文摘AIM: To study the antitumor effect of matrine in human hepatoma G2 (HepG2) cells and its molecular mechanism involved in antineoplastic activities. METHODS: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect viability of HepG2 cells. The effect of matrine on cell cycle was detected by flow cytometry. Annexin-V-FITC/PI double staining assay was used to detect cellular apoptosis. Cellular morphological changes were observed under an inverted phase contrast microscope. Transmission electron microscopy was performed to further examine ultrastructural structure of the cells treatedwith matrine. Monodansylcadaverine (MDC) staining was used to detect autophagy. Whether autophagy is blocked by 3-methyladenine (3-MA), an autophagy inhibitor, was evaluated. Expression levels of Bax and Beclin 1 in HepG2 cells were measured by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR).RESULTS: Matrine signif icantly inhibited the proliferation of HepG2 cells in a dose- and time-dependent manner, and induced G1-phase cell cycle arrest and apoptosis of HepG2 cells in a dose-dependent manner. The total apoptosis rate was 0.14% for HepG2 cells not treated with matrine. In contrast, the apoptosis rate was 28.91%, 34.36% and 38.80%, respectively, for HepG2 cells treated with matrine at the concentration of 0.5, 1.0 and 2.0 mg/mL. The remarkable morphological changes were observed under an inverted phase contrast microscope. Abundant cytoplasmic vacuoles with varying sizes were observed in HepG2 cells treated with matrine. Furthermore, vacuolization in cytoplasm progressively became larger and denser when the concentration of matrine was increased. Electron microscopy demonstrated formation of abundant autophagic vacuoles in HepG2 cells after matrine treatment. When the specif ic autophagic inhibitor, 3-MA, was applied, the number of autophagic vacuoles greatly decreased. MDC staining showed that the fluorescent density was higher and the number of MDC-labeled particles in HepG2 cells was greater in matrine treatment group than in control group. Fewer autophagic vacuoles were observed in the combined 3-MA and matrine treatment group when 3-MA was added before matrine treatment, indicating that both autophagy and apoptosis are activated when matrine-induced death of hepatoma G2 cells occurs. Real-time quantitative RT-PCR revealed that the expression levels of Bax gene, an apoptosis-related molecule, and Beclin 1 gene which plays a key role in autophagy were higher in matrine treatment group than in control group, indicating that Beclin 1 is involved in matrineinduced autophagy and the pro-apoptotic mechanismof matrine may be related to its upregulation of Bax expression. CONCLUSION: Matrine has potent antitumor activities in HepG2 cells and may be used as a novel effective reagent in treatment of hepatocellular carcinoma. | Zhang, Jun-Qiang Li, Yu-Min Liu, Tao He, Wen-Ting Chen, Ying-Tai Chen, Xiao-Hui Li, Xun Zhou, Wen-Ce Yi, Jian-Feng Ren, Zhi-Jian | 2010 | World Journal of Gastroenterology2010，16，34： | 61 |
| 4 | Autophagy and multidrug resistance in cancer显示文摘Multidrug resistance(MDR) occurs frequently after long-term chemotherapy, resulting in refractory cancer and tumor recurrence.Therefore, combatting MDR is an important issue. Autophagy, a self-degradative system, universally arises during the treatment of sensitive and MDR cancer. Autophagy can be a double-edged sword for MDR tumors: it participates in the development of MDR and protects cancer cells from chemotherapeutics but can also kill MDR cancer cells in which apoptosis pathways are inactive. Autophagy induced by anticancer drugs could also activate apoptosis signaling pathways in MDR cells, facilitating MDR reversal. Therefore, research on the regulation of autophagy to combat MDR is expanding and is becoming increasingly important. We summarize advanced studies of autophagy in MDR tumors, including the variable role of autophagy in MDR cancer cells. | Ying-Jie Li Yu-He Lei Nan Yao Chen-Ran Wang Nan Hu Wen-Cai Ye Dong-Mei Zhang Zhe-Sheng Chen | 2017 | Chinese Journal of Cancer2017，36，8： | 54 |
| 5 | Role of autophagy in tumorigenesis,metastasis,targeted therapy and drug resistance of hepatocellular carcinoma显示文摘Autophagy is a 'self-degradative' process and is involved in the maintenance of cellular homeostasis and the control of cellular components by facilitating the clearance or turnover of long-lived or misfolded proteins, protein aggregates, and damaged organelles. Autophagy plays a dual role in cancer, including in tumor progression and tumor promotion, suggesting that autophagy acts as a double-edged sword in cancer cells. Liver cancer is one of the greatest leading causes of cancer death worldwide due to its high recurrence rate and poor prognosis. Especially in China, liver cancer has become one of the most common cancers due to the high infection rate of hepatitis virus. In primary liver cancer, hepatocellular carcinoma (HCC) is the most common type. Considering the perniciousness and complexity of HCC, it is essential to elucidate the function of autophagy in HCC. In this review, we summarize the physiological function of autophagy in cancer, analyze the role of autophagy in tumorigenesis and metastasis, discuss the therapeutic strategies targeting autophagy and the mechanisms of drug-resistance in HCC, and provide potential methods to circumvent resistance and combined anticancer strategies for HCC patients. | Fang Huang Bing-Rong Wang Yi-Gang Wang | 2018 | World Journal of Gastroenterology2018，24，41： | 37 |
| 6 | Autophagy: novel insights into therapeutic target of electroacupuncture against cerebral ischemia/reperfusion injury显示文摘Electroacupuncture is known as an effective adjuvant therapy in ischemic cerebrovascular disease. However, its underlying mechanisms remain unclear. Studies suggest that autophagy, which is essential for cell survival and cell death, is involved in cerebral ischemia reperfusion injury and might be modulate by electroacupuncture therapy in key ways. This paper aims to provide novel insights into a therapeutic target of electroacupuncture against cerebral ischemia/reperfusion injury from the perspective of autophagy. Here we review recent studies on electroacupuncture regulation of autophagy-related markers such as UNC-51-like kinase-1 complex, Beclin1, microtubule-associated protein-1 light chain 3, p62, and autophagosomes for treating cerebral ischemia/reperfusion injury. The results of these studies show that electroacupuncture may affect the initiation of autophagy, vesicle nucleation, expansion and maturation of autophagosomes, as well as fusion and degradation of autophagolysosomes. Moreover, studies indicate that electroacupuncture probably modulates autophagy by activating the mammalian target of the rapamycin signaling pathway.This review thus indicates that autophagy is a therapeutic target of electroacupuncture treatment against ischemic cerebrovascular diseases. | Ya-Guang Huang Wei Tao Song-Bai Yang Jin-Feng Wang Zhi-Gang Mei Zhi-Tao Feng | 2019 | Neural Regeneration Research2019，14，6： | 39 |
| 7 | Apelin-13 inhibits apoptosis and excessive autophagy in cerebral ischemia/reperfusion injury显示文摘Apelin-13 is a novel endogenous ligand for an angiotensin-like orphan G-protein coupled receptor,and it may be neuroprotective against cerebral ischemia injury.However,the precise mechanisms of the effects of apelin-13 remain to be elucidated.To investigate the effects of apelin-13 on apoptosis and autophagy in models of cerebral ischemia/reperfusion injury,a rat model was established by middle cerebral artery occlusion.Apelin-13(50μg/kg)was injected into the right ventricle as a treatment.In addition,an SH-SY5Y cell model was established by oxygen-glucose deprivation/reperfusion,with cells first cultured in sugar-free medium with 95%N2 and 5%CO2 for 4 hours and then cultured in a normal environment with sugar-containing medium for 5 hours.This SH-SY5Y cell model was treated with 10-7 M apelin-13 for 5 hours.Results showed that apelin-13 protected against cerebral ischemia/reperfusion injury.Apelin-13 treatment alleviated neuronal apoptosis by increasing the ratio of Bcl-2/Bax and significantly decreasing cleaved caspase-3 expression.In addition,apelin-13 significantly inhibited excessive autophagy by regulating the expression of LC3B,p62,and Beclin1.Furthermore,the expression of Bcl-2 and the phosphatidylinositol-3-kinase(PI3K)/Akt/mammalian target of rapamycin(mTOR)pathway was markedly increased.Both LY294002(20μM)and rapamycin(500 nM),which are inhibitors of the PI3K/Akt/mTOR pathway,significantly attenuated the inhibition of autophagy and apoptosis caused by apelin-13.In conclusion,the findings of the present study suggest that Bcl-2 upregulation and mTOR signaling pathway activation lead to the inhibition of apoptosis and excessive autophagy.These effects are involved in apelin-13-induced neuroprotection against cerebral ischemia/reperfusion injury,both in vivo and in vitro.The study was approved by the Animal Ethical and Welfare Committee of Jining Medical University,China(approval No.2018-JS-001)in February 2018. | Zi-Qi Shao Shan-Shan Dou Jun-Ge Zhu Hui-Qing Wang Chun-Mei Wang Bao-Hua Cheng Bo Bai | 2021 | Neural Regeneration Research2021，16，6： | 35 |
| 8 | Apoptosis and non-alcoholic fatty liver diseases显示文摘The number of patients with nonalcoholic fatty liver diseases(NAFLD) including nonalcoholic steatohepatitis(NASH), has been increasing. NASH causes cirrhosis and hepatocellular carcinoma(HCC) and is one of the most serious health problems in the world. The mechanism through which NASH progresses is still largely unknown. Activation of caspases, Bcl-2 family proteins, and c-Jun N-terminal kinase-induced hepatocyte apoptosis plays a role in the activation of NAFLD/NASH. Apoptotic hepatocytes stimulate immune cells and hepatic stellate cells toward the progression of fibrosis in the liver through the production of inflammasomes and cytokines. Abnormalities in glucose and lipid metabolism as well as microbiota accelerate these processes. The production of reactive oxygen species, oxidative stress, and endoplasmic reticulum stress is also involved. Cell death, including apoptosis, seems very important in the progression of NAFLD and NASH. Recently, inhibitors of apoptosis have been developed as drugs for the treatment of NASH and may prevent cirrhosis and HCC. Increased hepatocyte apoptosis may distinguish NASH from NAFLD, and the improvement of apoptosis could play a role in controlling the development of NASH. In this review, the association between apoptosis and NAFLD/NASH are discussed. This review could provide their knowledge, which plays a role in seeing the patients with NAFLD/NASH in daily clinical practice. | Tatsuo Kanda Shunichi Matsuoka Motomi Yamazaki Toshikatsu Shibata Kazushige Nirei Hiroshi Takahashi Tomohiro Kaneko Mariko Fujisawa Teruhisa Higuchi Hitomi Nakamura Naoki Matsumoto Hiroaki Yamagami Masahiro Ogawa Hiroo Imazu Kazumichi Kuroda Mitsuhiko Moriyama | 2018 | World Journal of Gastroenterology2018，24，25： | 32 |
| 9 | Regulation of multidrug resistance by microRNAs in anti-cancer therapy显示文摘Multidrug resistance(MDR) remains a major clinical obstacle to successful cancer treatment.Although diverse mechanisms of MDR have been well elucidated, such as dysregulation of drugs transporters, defects of apoptosis and autophagy machinery, alterations of drug metabolism and drug targets, disrupti on of redox homeostasis, the exact mechanisms of MDR in a specific cancer patient and the cross-talk among these different mechanisms and how they are regulated are poorly understood.Micro RNAs(mi RNAs) are a new class of small noncoding RNAs that could control the global activity of the cell by post-transcriptionally regulating a large variety of target genes and proteins expression.Accumulating evidence shows that mi RNAs play a key regulatory role in MDR through modulating various drug resistant mechanisms mentioned above, thereby holding much promise for developing novel and more effective individualized therapies for cancer treatment. This review summarizes the various MDR mechanisms and mainly focuses on the role of mi RNAs in regulating MDR in cancer treatment. | Xin An Cesar Sarmiento Tao Tan Hua Zhu | 2017 | Acta Pharmaceutica Sinica B2017，7，1： | 29 |
| 10 | Mechanisms of drug resistance in colon cancer and its therapeutic strategies显示文摘Drug resistance develops in nearly all patients with colon cancer, leading to a decrease in the therapeutic efficacies of anticancer agents. This review provides an up-to-date summary on over-expression of ATPbinding cassette(ABC) transporters and evasion of apoptosis, two representatives of transport-based and non-transport-based mechanisms of drug resistance, as well as their therapeutic strategies. Different ABC transporters were found to be up-regulated in colon cancer, which can facilitate the efflux of anticancer drugs out of cancer cells and decrease their therapeutic effects. Inhibition of ABC transporters by suppressing their protein expressions or co-administration of modulators has been proven as an effective approach to sensitize drug-resistant cancer cells to anticancer drugs in vitro. On the other hand, evasion of apoptosis observed in drug-resistant cancers also results in drug resistance to anticancer agents, especially to apoptosis inducers. Restoration of apoptotic signals by BH3 mimetics or epidermal growth factor receptor inhibitors and inhibition of cancer cell growth by alternative cell death pathways, such as autophagy, are effective means to treat such resistant cancer types. Given that the drug resistance mechanisms are different among colon cancer patients and may change even in a single patient at different stages, personalized and specific combination therapy is proposed to be more effective and safer for the reversal of drug resistance in clinics. | Tao Hu Zhen Li Chun-Ying Gao Chi Hin Cho | 2016 | World Journal of Gastroenterology2016，22，30： | 29 |
| 11 | Hepatocellular carcinoma redirects to ketolysis for progression under nutrition deprivation stress显示文摘癌症房间以他们的能力著名给新陈代谢的小径换新电线在各种各样的压力条件下面支持幸存和增长。尽管在肝生产了,酉同类身体没在正常的成年的肝房间被消费。我们这里发现酉同类分解代谢或 ketolysis 在 hepatocellular 被重新激活在营养剥夺条件下面的癌(HCC ) 房间。机械学地, 3-oxoacid CoA-transferase 1 (OXCT1 ) ,其表情在正常的成年的肝纸巾被压制的限制率的 ketolytic 酶,被浆液重新导致被触发饥饿的 mTORC2-AKT-SP1 在 HCC 房间发信号。而且,我们观察到在 HCC 的那提高的 ketolysis 为 AMPK 激活的压抑是批评的并且保护 HCC 房间免受过多的 autophagy 的伤害,从而提高肿瘤生长。重要地,临床的 HCC 样品的分析表明那增加的 OXCT1 表情预言更高耐心的死亡。一起拿,我们这里揭开剥夺营养的 HCC 房间为精力由采用酉同类身体的新奇新陈代谢的改编供应和癌症前进。 | De Huang Tingting Li Lin Wang Long Zhang Ronghui Yan Kui Li Songge Xing Gongwei Wu Lan Hu Weidong Jia Sheng-Cai Lin Chi V Dang Libing Song Ping Gao Huafeng Zhang | 2016 | Cell Research2016，26，10： | 27 |
| 12 | Role of autophagy in the pathogenesis of inflammatory bowel disease显示文摘Inflammatory bowel disease(IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system.Recently, some studies provided strong evidence that the process of autophagy affects several aspects of mucosal immune responses. Autophagy is a cellular stress response that plays key roles in physiological processes, such as innate and adaptive immunity, adaptation to starvation, degradation of aberrant proteins or organelles, antimicrobial defense, and protein secretion. Dysfunctional autophagy is recognized as a contributing factor in many chronic inflammatory diseases, including IBD. Autophagy plays multiple roles in IBD pathogenesis by altering processes that include intracellular bacterial killing, antimicrobial peptide secretion by Paneth cells, goblet cell function, proinflammatory cytokine production by macrophages, antigen presentation by dendritic cells, and the endoplasmic reticulum stress response in enterocytes. Recent studies have identified susceptibility genes involved in autophagy, such as NOD2, ATG16L1, and IRGM, and active research is ongoing all over the world. The aim of this review is a systematic appraisal of the current literature to provide a better understanding of the role of autophagy in the pathogenesis of IBD. Understanding these mechanisms will bring about new strategies for the treatment and prevention of IBD. | Tomoya Iida Kei Onodera Hiroshi Nakase | 2017 | World Journal of Gastroenterology2017，23，11： | 27 |
| 13 | Neuronal autophagy aggravates microglial inflammatory injury by downregulating CX3CL1/fractalkine after ischemic stroke显示文摘Ischemic stroke often induces excessive neuronal autophagy, resulting in brain damage; meanwhile, inflammatory responses stimulated by ischemia exacerbate neural injury. However, interactions between neuronal autophagy and microglial inflammation following ischemic stroke are poorly understood. CX3CL1/fractalkine, a membrane-bound chemokine expressed on neurons, can suppress microglial inflammation by binding to its receptor CX3CR1 on microglia. In the present study, to investigate whether autophagy could alter CX3CL1 expression on neurons and consequently change microglial inflammatory activity, middle cerebral artery occlusion(MCAO) was established in Sprague-Dawley rats to model ischemic stroke, and tissues from the ischemic penumbra were obtained to evaluate autophagy level and microglial inflammatory activity. MCAO rats were administered 3-methyladenine(autophagy inhibitor) or Tat-Beclin 1(autophagy inducer). Western blot assays were conducted to quantify expression of Beclin-1, nuclear factor kappa Bp65(NF-κB), light chain 3B(LC3B), and CX3CL1 in ischemic penumbra. Moreover, immunofluorescence staining was performed to quantify numbers of LC3B-, CX3CL1-, and Iba-1-positive cells in ischemic penumbra. In addition, enzyme linked immunosorbent assays were utilized to analyze concentrations of tumor necrosis factor alpha(TNF-α), interleukin 6(IL-6), interleukin 1 beta(IL-1β), and prostaglandin E2(PGE2). A dry/wet weight method was used to detect brain water content, while 2,3,5,-triphenyltetrazolium chloride staining was utilized to measure infarct volume. The results demonstrated that autophagy signaling(Beclin-1 and LC3B expression) in penumbra was prominently activated by MCAO, while CX3CL1 expression on autophagic neurons was significantly reduced and microglial inflammation was markedly activated. However, after inhibition of autophagy signaling with 3-methyladenine, CX3CL1 expression on neurons was obviously increased, whereas Iba-1 and NF-κB expression was downregulated; TNF-α, IL-6, IL-1β, and PGE2 levels were decreased; and cerebral edema was obviously mitigated. In contrast, after treatment with the autophagy inducer Tat-Beclin 1, CX3CL1 expression on neurons was further reduced; Iba-1 and NF-κB expression was increased; TNF-α, IL-6, IL-1β, and PGE2 levels were enhanced; and cerebral edema was aggravated. Our study suggests that ischemia-induced neuronal autophagy facilitates microglial inflammatory injury after ischemic stroke, and the efficacy of this process may be associated with downregulated CX3CL1 expression on autophagic neurons. | Hong-Yun He Lu Ren Tao Guo Yi-Hao Deng | 2019 | Neural Regeneration Research2019，14，2： | 25 |
| 14 | Autophagy in bone homeostasis and the onset of osteoporosis显示文摘Autophagy is an evolutionarily conserved intracellular process,in which domestic cellular components are selectively digested for the recycling of nutrients and energy.This process is indispensable for cell homeostasis maintenance and stress responses.Both genetic and functional studies have demonstrated that multiple proteins involved in autophagic activities are critical to the survival,differentiation,and functioning of bone cells,including osteoblasts,osteocytes,and osteoclasts.Dysregulation at the level of autophagic activity consequently disturbs the balance between bone formation and bone resorption and mediates the onset and progression of multiple bone diseases,including osteoporosis.This review aims to introduce the topic of autophagy,summarize the understanding of its relevance in bone physiology,and discuss its role in the onset of osteoporosis and therapeutic potential. | Xing Yin Chenchen Zhou Jingtao Li Renkai Liu Bing Shi Quan Yuan Shujuan Zou | 2019 | Bone Research2019，7，4： | 25 |
| 15 | Jianpi Qingchang decoction regulates intestinal motility of dextran sulfate sodium-induced colitis through reducing autophagy of interstitial cells of Cajal显示文摘AIM To investigate the underlying effect of Jianpi Qingchang decoction(JQD) regulating intestinal motility of dextran sulfate sodium(DSS)-induced colitis in mice. METHODS C57BL/6 mice were randomly divided into four groups: the control group, the DSS group, the JQD group, and the 5-aminosalicylic acid group. Except for the control group, colitis was induced in other groups by giving distilled water containing 5% DSS. Seven days after modeling, the mice were administered corresponding drugs intragastrically. The mice were sacrificed on the 15^(th) day. The disease activity index, macroscopic and histopathologic lesions, and ultrastructure of colon interstitial cells of Cajal(ICC) were observed. The levels of tumor necrosis factor-alpha(TNF-α), interleukin(IL)-1β, IL-10 and interferon gamma(IFN-γ), the expression of nuclear factor-kappa B(NF-κB) p65, c-kit, microtubule-associated protein 1 light chain 3(LC3-Ⅱ) and Beclin-l m RNA, and the colonic smooth muscle tension were assessed. RESULTS Acute inflammation occurred in the mice administered DSS. Compared with the control group, the levels of IL-1β, TNF-α, IL-10 and IFN-γ, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency increased(P < 0.05), the expression of c-kit m RNA and the colonic smooth muscle contractile amplitude decreased in the DSS group(P < 0.05). Compared with the DSS group, the levels of IL-10 and IFN-γ, the expression of c-kit m RNA, and the colonic smooth muscle contractile amplitude increased(P < 0.05), the levels of TNF-α and IL-1β, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency decreased in the JQD group(P < 0.05).CONCLUSION JQD can regulate the intestinal motility of DSS-induced colitis in mice through suppressing intestinal inflammatory cascade reaction, reducing autophagy of ICC, and regulating the network path of ICC/smooth muscle cells. | Yan-Cheng Dai Lie Zheng Ya-Li Zhang Xuan Chen De-Liang Chen Li-Juan Wang Zhi-Peng Tang | 2017 | World Journal of Gastroenterology2017，23，26： | 26 |
| 16 | Inhibiting effect of Endostar combined with ginsenoside Rg3 on breast cancer tumor growth in tumor-bearing mice显示文摘Objective: To study the inhibiting effect of Endostar combined with ginsenoside Rg3 on breast cancer tumor growth in tumor-bearing mice. Methods: Female mice were selected as experimental animals, and breast cancer tumor-bearing mouse models were established and then divided into group A, B, C and D that respectively received saline, recombinant human endostatin, ginsenosides Rg3 and recombinant human endostatin combined with Rg3 intervention; 7 d, 14 d and 21 d after intervention, tumor tissue volume was measured; 21 d after intervention, mice were killed, tumor tissue was collected, and m RNA contents of angiogenesis molecules, invasion molecules, autophagy marker molecules and autophagy signaling pathway molecules were detected. Results: At 7 d, 14 d and 21 d after intervention, tumor tissue volume of group B, C and D was lower than that of group A, and tumor tissue volume of group D was lower than that of group B and C; m RNA contents of VEGFA, VEGFB, VEGFC, MMP2, MMP9, p62, m TOR, PI3 K, Akt, JNK and Beclin-1 in tumor tissue of group B, C and D were significantly lower than those of group A, and LC3-II/LC3-I was significantly higher than that of group A; m RNA contents of VEGFA, VEGFB, VEGFC, MMP2, MMP9, p62, m TOR, PI3 K, Akt, JNK and Beclin-1 in tumor tissue of group D were significantly lower than those of group B and C, and LC3-II/LC3-I was higher than that of group B and C. Conclusions: Endostar combined with ginsenoside Rg3 has stronger inhibiting effect on breast cancer tumor growth in tumor-bearing mice than single drug, and it can inhibit angiogenesis and cell invasion, and enhance cell autophagy. | Yun Zhang Qing-Zhan Liu Su-Ping Xing Jin-Ling Zhang | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，2： | 24 |
| 17 | 5'-Monophosphate-activated protein kinase (AMPK) improves autophagic activity in diabetes and diabetic complications显示文摘Diabetes mellitus(DM),an endocrine disorder,will be one of the leading causes of death world-wide in about two decades.Cellular injuries and disorders of energy metabolism are two key factors in the pathogenesis of diabetes,which also become the important causes for the process of diabetic complications.AMPK is a key enzyme in maintaining metabolic homeostasis and has been implicated in the activation of autophagy in distinct tissues.An increasing number of researchers have confirmed that autophagy is a potential factor to affect or induce diabetes and its complications nowadays,which could remove cytotoxic proteins and dysfunctional organelles.This review will summarize the regulation of autophagy and AMPK in diabetes and its complications,and explore how AMPK stimulates autophagy in different diabetic syndromes.A deeper understanding of the regulation and activity of AMPK in autophagy would enhance its development as a promising therapeutic target for diabetes treatment. | Fan Yao Ming Zhang Li Chen | 2016 | Acta Pharmaceutica Sinica B2016，6，1： | 24 |
| 18 | The crosstalk between autophagy and apoptosis: where does this lead?显示文摘Recent advances in the understanding of the molecular processes contributing to autophagy have provided insight into the relationship between autophagy and apoptosis.In contrast to the concept of“autophagic cell death,”accumulating evidence suggests that autophagy serves a largely cytoprotective role in physiologically relevant conditions.The cytoprotective function of autophagy is mediated in many circumstances by negative modulation of apoptosis.Apoptotic signaling,in turn,serves to inhibit autophagy.While the mechanisms mediating the complex counter-regulation of apoptosis and autophagy are not yet fully understood,important points of crosstalk include the interactions between Beclin-1 and Bcl-2/Bcl-xL and between FADD and Atg5,caspase-and calpain-mediated cleavage of autophagy-related proteins,and autophagic degradation of caspases.Continued investigation of these and other means of crosstalk between apoptosis and autophagy is necessary to elucidate the mechanisms controlling the balance between survival and death both under normal conditions and in diseases including cancer. | Claire Gordy You-Wen He | 2012 | Protein & Cell2012，3，1： | 23 |
| 19 | LncRNA-ATB promotes autophagy by activating Yes-associated protein and inducing autophagy-related protein 5 expression in hepatocellular carcinoma显示文摘BACKGROUND Long non-coding RNAs (lncRNAs) play important roles in many diseases, including hepatocellular carcinoma (HCC). Autophagy is a metabolic pathway that facilitates cancer cell survival in response to stress. The relationship between autophagy and the lncRNA-activated by transforming growth factor beta (lncRNA-ATB) in HCC remains unknown. AIM To explore the influence of lncRNA-ATB in regulating autophagy in HCC cells and the underlying mechanism. METHODS In the present study, we evaluated lncRNA-ATB expression in tumor and adjacent non-tumor tissues from 72 HCC cases by real-time PCR. We evaluated the role of lncRNA-ATB in the proliferation and clonogenicity of HCC cells in vitro. The effect of lncRNA-ATB on autophagy was determined using a LC3-GFP reporter and transmission electron microscopy. Furthermore, the mechanism by which lncRNA-ATB regulates autophagy was explored by immunofluorescence staining, RNA immunoprecipitation (RIP), and Western blot. RESULTS The expression of lncRNA-ATB was higher in HCC tissues than in normal liver tissues, and lncRNA-ATB expression was positively correlated with tumor size, TNM stage, and poorer survival of patients with HCC. Moreover, ectopic overexpression of lncRNA-ATB promoted cell proliferation and clonogenicnity of HCC cells in vitro. LncRNA-ATB promoted autophagy by activating Yesassociated protein (YAP). Moreover, lncRNA-ATB interacted with autophagy-related protein 5 (ATG5) mRNA and increased ATG5 expression. CONCLUSION LncRNA-ATB regulates autophagy by activating YAP and increasing ATG5 expression. Our data demonstrate a novel function for lncRNA-ATB in autophagy and suggest that lncRNA-ATB plays an important role in HCC. | Chuan-Zhuo Wang Guang-Xin Yan De-Shuo Dong He Xin Zhao-Yu Liu | 2019 | World Journal of Gastroenterology2019，25，35： | 21 |
| 20 | Sevoflurane postconditioning protects against myocardial ischemia/reperfusion injury by restoring autophagic flux via an NO-dependent mechanism显示文摘Volatile anesthetics improve postischemic cardiac function and reduce infarction even when administered for only a brief-time at the onset of reperfusion.A recent study showed that sevoflurane postconditioning (SPC)attenuated myocardial reperfusion injury, but the underlying mechanisms remain unclear,in this study,we examined the effects of sevoflurane on nitric oxide (NO)release and autophagic flux during the myocardial ischemia/reperfusion (I/R)injury in rats in vivo and ex vivo.Male rats were subjected to 30 min ischemia and 2 h reperfusion in the presence or absence of sevoflurane (1.0 minimum alveolar concentration)during the first 15 min of reperfusion.We found that SPC significantly improved hemodynamic performance after reperfusion,alleviated postischemic myocardial infarction,reduced nicotinamide adenine dinucleotide content loss,and cytochrome c.release in heart tissues.Furthermore,SPC significantly increased the phosphorylation of endothelial nitric oxide synthase (NOS)and neuronal nitric oxide synthase,and elevated myocardial NOS activity and NO production.All these effects were abolished by treatment with an NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME,10 mg/kg,i.v.).We also observed myocardial I/R-induced accumulation of autophagosomes in heart tissues,as evidenced by increased ratios of microtubule:associated protein 1 light chain 3 Ⅱ/Ⅰ,upregulation of Beclin 1 and P62,and reduced lysosome-assciated membrane protein-2 expression.SPC significantly attenuated I/R- impaired autophagic flux,which were blocked by L-NAME.Moreover,pretreatment with the autophagic flUX blocker chloroquine (10 mg/kg,i.p.)increased autophagosome accumulation in SPC-treated heart following I/R and blocked SPC-induced cardioprotection.The same results were also observed in a rat model of myocardial I/R injury ex vivo,suggesting that SPC protects rat hearts against myocardial reperfusion injury by restoring I/R-impaired autophagic flux yia an NO-dependent mechanism. | Shi-gang Qiao Ying Sun Bo Sun An Wang Jia Qiu Lei Hong Jian-zhong An Chen Wang Hui-ling Zhang | 2019 | Acta Pharmacologica Sinica2019，40，1： | 21 |
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