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| 1 | Elevated exhaustion levels and reduced functional diversity of T cells in peripheral blood may predict severe progression in COVID-19 patients显示文摘The novel contagious primary atypical pneumonia epidemic,which broke out in Wuhan,China,in December 2019,is now formally called Coronavirus Disease 2019(COVID-19),with the causative virus named as Severe Acute Respiratory Syndrome Coronavirus 2(SARS-CoV-2).1,2 Recent studies have shown that in addition to dyspnea,hypoxemia,and acute respiratory distress,lymphopenia,and cytokine release syndrome are also important clinical features in patients with severe SARS-CoV-2 infection.3 This suggests that homeostasis of the immune system plays an important role in the development of COVID-19 pneumonia. | Hong-Yi Zheng Mi Zhang Cui-Xian Yang Nian Zhang Xi-Cheng Wang Xin-Ping Yang Xing-Qi Dong Yong-Tang Zheng | 2020 | Cellular & Molecular Immunology2020，17，5： | 38 |
| 2 | Targeting NF-κB pathway for the therapy of diseases:mechanism and clinical study显示文摘NF-κB pathway consists of canonical and non-canonical pathways.The canonical NF-κB is activated by various stimuli,transducing a quick but transient transcriptional activity,to regulate the expression of various proinflammatory genes and also serve as the critical mediator for inflammatory response.Meanwhile,the activation of the non-canonical NF-κB pathway occurs through a handful of TNF receptor superfamily members.Since the activation of this pathway involves protein synthesis,the kinetics of non-canonical NF-κB activation is slow but persistent,in concordance with its biological functions in the development of immune cell and lymphoid organ,immune homeostasis and immune response.The activation of the canonical and non-canonical NF-κB pathway is tightly controlled,highlighting the vital roles of ubiquitination in these pathways.Emerging studies indicate that dysregulated NF-κB activity causes inflammation-related diseases as well as cancers,and NF-κB has been long proposed as the potential target for therapy of diseases.This review attempts to summarize our current knowledge and updates on the mechanisms of NF-κB pathway regulation and the potential therapeutic application of inhibition of NF-κB signaling in cancer and inflammatory diseases. | Hui Yu Liangbin Lin Zhiqiang Zhang Huiyuan Zhang Hongbo Hu | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 35 |
| 3 | Role of adipokines and peroxisome proliferator-activated receptors in nonalcoholic fatty liver disease显示文摘Intrahepatic fat deposition has been demonstrated in patients with nonalcoholic fatty liver disease(NAFLD). Genetic and environmental factors are important for the development of NAFLD. Diseases such as obesity, diabetes, and hypertension have been found to be closely associated with the incidence of NAFLD. Evi-dence suggests that obesity and insulin resistance are the major factors that contribute to the development of NAFLD. In comparing the factors that contribute to the buildup of excess calories in obesity, an imbalance of energy homeostasis can be considered as the basis. Among the peripheral signals that are generated to regulate the uptake of food, signals from adipose tissue are of major relevance and involve the maintenance of energy homeostasis through processes such as lipo-genesis, lipolysis, and oxidation of fatty acids. Advances in research on adipose tissue suggest an integral role played by adipokines in NAFLD. Cytokines secreted by adipocytes, such as tumor necrosis factor-α, transform-ing growth factor-β, and interleukin-6, are implicated in NAFLD. Other adipokines, such as leptin and adiponectin and, to a lesser extent, resistin and retinol binding protein-4 are also involved. Leptin and adiponectin can augment the oxidation of fatty acid in liver by activating the nuclear receptor super-family of transcription fac-tors, namely peroxisome proliferator-activated receptor(PPAR)-α. Recent studies have proposed downregula-tion of PPAR-α in cases of hepatic steatosis. This re-view discusses the role of adipokines and PPARs with regard to hepatic energy metabolism and progression of NAFLD. | Vettickattuparambil George Giby Thekkuttuparambil Ananthanarayanan Ajith | 2014 | World Journal of Hepatology2014，6，8： | 30 |
| 4 | Wnt/β-catenin signalling:function,biological mechanisms,and therapeutic opportunities显示文摘The Wnt/β-catenin pathway comprises a family of proteins that play critical roles in embryonic development and adult tissue homeostasis.The deregulation of Wnt/β-catenin signalling often leads to various serious diseases,including cancer and non-cancer diseases.Although many articles have reviewed Wnt/β-catenin from various aspects,a systematic review encompassing the origin,composition,function,and clinical trials of the Wnt/β-catenin signalling pathway in tumour and diseases is lacking.In this article,we comprehensively review the Wnt/β-catenin pathway from the above five aspects in combination with the latest research.Finally,we propose challenges and opportunities for the development of small-molecular compounds targeting the Wnt signalling pathway in disease treatment. | Jiaqi Liu Qing Xiao Jiani Xiao Chenxi Niu Yuanyuan Li Xiaojun Zhang Zhengwei Zhou Guang Shu Gang Yin | 2022 | Signal Transduction and Targeted Therapy2022，7，2： | 28 |
| 5 | Unconjugated bilirubin alleviates experimental ulcerative colitis by regulating intestinal barrier function and immune inflammation显示文摘BACKGROUND Unconjugated bilirubin(UCB) is generally considered toxic but has gained recent prominence for its anti-inflammatory properties. However, the effects of it on the interaction between intestinal flora and organisms and how it influences immune responses remain unresolved.AIM To investigate the role of UCB in intestinal barrier function and immune inflammation in mice with dextran-sulfate-sodium-induced colitis.METHODS Acute colitis was induced by 3%(w/v) dextran sulfate sodium salt in drinking water for 6 d followed by untreated water for 2 d. Concurrently, mice with colitis were administered 0.2 mL UCB(400 μmol/L) by intra-gastric gavage for 7 d.Disease activity index(DAI) was monitored daily. Mice were sacrificed at the end of the experiment. The length of the colon and weight of the spleen were recorded. Serum level of D-lactate, intestinal digestive proteases activity, and changes to the gut flora were analyzed. In addition, colonic specimens were analyzed by histology and for expression of inflammatory markers and proteins.RESULTS Mice treated with UCB had significantly relieved severity of colitis, including lower DAI, longer colon length, and lower spleen weight(colon length: 4.92 ±0.09 cm vs 3.9 ± 0.15 cm; spleen weight: 0.33 ± 0.04 vs 0.74 ± 0.04, P < 0.001). UCB administration inactivated digestive proteases(chymotrypsin: 18.70 ± 0.69 U/g vs44.81 ± 8.60 U/g; trypsin: 1.52 ± 0.23 U/g vs 9.05 ± 1.77 U/g, P < 0.01), increased expression of tight junction(0.99 ± 0.05 vs 0.57 ± 0.03, P < 0.001), decreased serum level of D-lactate(31.76 ± 3.37 μmol/L vs 54.25 ± 1.45 μmol/L, P < 0.001), and lowered histopathological score(4 ± 0.57 vs 7 ± 0.57, P < 0.001) and activity of myeloperoxidase(46.79 ± 2.57 U/g vs 110.32 ± 19.19 U/g, P < 0.001). UCB also regulated the intestinal microbiota, inhibited expression of tumor necrosis factor(TNF) α and interleukin 1β(TNF-α: 52.61 ± 7.81 pg/mg vs 105.04 ± 11.92 pg/mg,interleukin 1β: 13.43 ± 1.68 vs 32.41 ± 4.62 pg/mg, P < 0.001), decreased expression of Toll-like receptor 4(0.61 ± 0.09 vs 1.07 ± 0.03, P < 0.001) and myeloid differentiation primary response gene 88(0.73 ± 0.08 vs 1.01 ± 0.07, P <0.05), and increased expression of TNF-receptor-associated factor 6(0.79 ± 0.02 vs0.43 ± 0.09 P < 0.05) and inhibitor of kappa B α(0.93 ± 0.07 vs 0.72 ± 0.07, P < 0.05)in the colon.CONCLUSION UCB can protect intestinal barrier function, regulate normal intestinal homeostasis, and suppress inflammation via the Toll-like receptor 4/nuclear factor-κB signaling pathway. | Jia-Dong Zheng Yan He Heng-Yuan Yu Yuan-Li Liu Yi-Xuan Ge Xue-Ting Li Xue Li Yan Wang Meng-Ru Guo Yi-Lin Qu Xiao-Fa Qin Ming-Shan Jiang Xiu-Hong Wang | 2019 | World Journal of Gastroenterology2019，25，15： | 26 |
| 6 | 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 |
| 7 | MAPK signaling in inflammation-associated cancer development显示文摘Mitogen-activated protein(MAP)kinases comprise a family of protein-serine/threonine kinases,which are highly conserved in protein structures from unicellular eukaryotic organisms to multicellular organisms,including mammals.These kinases,including ERKs,JNKs and p38s,are regulated by a phosphorelay cascade,with a prototype of three protein kinases that sequentially phosphorylate one another.MAPKs transduce extracellular signals into a variety of cellular processes,such as cell proliferation,survival,death,and differentiation.Consistent with their essential cellular functions,MAPKs have been shown to play critical roles in embryonic development,adult tissue homeostasis and various pathologies.In this review,we discuss recent findings that reveal the profound impact of these pathways on chronic inflammation and,particularly,inflammation-associated cancer development. | Pengyu Huang Jiahuai Han Lijian Hui | 2010 | Protein & Cell2010，1，3： | 25 |
| 8 | Restoring homeostasis of CD4^+ T cells in hepatitis-B-virusrelated liver fibrosis显示文摘Immune-mediated liver injury is widely seen during hepatitis B virus(HBV) infection. Unsuccessful immune clearance of HBV results in chronic hepatitis and increases the risk of liver cirrhosis and hepatocellular carcinoma. HBV-related liver fibrosis(HBVLF),occurring as a result of HBV-induced chronic hepatitis,is a reversible,intermediate stage of chronic hepatitis B(CHB) and liver cirrhosis. Therefore,defining the pathogenesis of HBVLF is of practical significance for achieving better clinical outcomes. Recently,the homeostasis of CD4+ T cells was considered to be pivotal in the process of HBVLF. To better uncover the underlying mechanisms,in this review,we systematically retrospect the impacts of different CD4+T-cell subsets on CHB and HBVLF. We emphasize CD4+ T-cell homeostasis and the important balance between regulatory T(Treg) and T helper 17(Th17) cells. We discuss some cytokines associated with Treg and Th17 cells such as interleukin(IL)-17,IL-22,IL-21,IL-23,IL-10,IL-35 and IL-33,as well as surface molecules such as programmed cell death protein 1,cytotoxic T lymphocyte-associated antigen 4,T cell immunoglobulin domain and mucin domain-containing molecule 3 and cannabinoid receptor 2 that have potential therapeutic implications for the homeostasis of CD4+ T cells in CHB and HBVLF. | Li-Sha Cheng Yun Liu Wei Jiang | 2015 | World Journal of Gastroenterology2015，21，38： | 26 |
| 9 | Metabolic consequences of Helicobacter pylori infection and eradication显示文摘Helicobacter pylori(H.pylori)is still the most prevalent infection of the world.Colonization of the stomach by this agent will invariably induce chronic gastritis which is a low-grade inflammatory state leading to local complications(peptic ulcer,gastric cancer,lymphoma)and remote manifestations.While H.pylori does not enter circulation,these extragastric manifestations are probably mediated by the cytokines and acute phase proteins produced by the inflammed mucosa.The epidemiologic link between the H.pylori infection and metabolic changes is inconstant and controversial.Growth delay was described mainly in low-income regions with high prevalence of the infection,where probably other nutritional and social factors contribute to it.The timely eradication of the infection will lead to a more healthy development of the young population,along with preventing peptic ulcers and gastric cancer An increase of total,low density lipoprotein and high density liporotein cholesterol levels in some infected people creates an atherogenic lipid profile which could promote atherosclerosis with its complications,myocardial infarction,stroke and peripheral vascular disease.Well designed and adequately powered long-term studies are required to see whether eradication of the infection will prevent these conditions.In case of glucose metabolism,the most consistent association was found between H.pylori and insulin resistance:again,proof that eradication prevents this common metabolic disturbance is expected.The results of eradication with standard regimens in diabetics are significantly worse than in non-diabetic patients,thus,more active regimens must be found to obtain better results.Successful eradication itself led to an increase of body mass index and cholesterol levels in some populations,while in others no such changes were encountered.Uncertainities of the metabolic consequences of H.pylori infection must be clarified in the future. | Gy?rgy Miklós Buzás | 2014 | World Journal of Gastroenterology2014，20，18： | 20 |
| 10 | Role of microbiota on lung homeostasis and diseases显示文摘The lungs, as a place of gas exchange, are continuously exposed to environmental stimuli, such as allergens, microbes, and pollutants. The development of the culture-independent technique for microbiological analysis, such as 16 S rRNA sequencing,has uncovered that the lungs are not sterile and, in fact, colonized by diverse communities of microbiota. The function of intestinal microbiota in modulating mucosal homeostasis and defense has been widely studied; however, the potential function of lung microbiota in regulating immunity and homeostasis has just begun. Increasing evidence indicates the relevance of microbiota to lung homeostasis and disease. In this review, we describe the distribution and composition of microbiota in the respiratory system and discuss the potential function of lung microbiota in both health and acute/chronic lung disease. In addition, we also discuss the recent understanding of the gut-lung axis, because several studies have revealed that the immunological interaction among the gut, the lung, and the microbiota was involved in this issue. | Jian Wang Fengqi Li Zhigang Tian | 2017 | Science China(Life Sciences)2017，60，12： | 18 |
| 11 | Notch signaling pathway:architecture,disease,and therapeutics显示文摘The NOTCH gene was identified approximately 110 years ago.Classical studies have revealed that NOTCH signaling is an evolutionarily conserved pathway.NOTCH receptors undergo three cleavages and translocate into the nucleus to regulate the transcription of target genes.NOTCH signaling deeply participates in the development and homeostasis of multiple tissues and organs,the aberration of which results in cancerous and noncancerous diseases.However,recent studies indicate that the outcomes of NOTCH signaling are changeable and highly dependent on context.In terms of cancers,NOTCH signaling can both promote and inhibit tumor development in various types of cancer.The overall performance of NOTCH-targeted therapies in clinical trials has failed to meet expectations.Additionally,NOTCH mutation has been proposed as a predictive biomarker for immune checkpoint blockade therapy in many cancers.Collectively,the NOTCH pathway needs to be integrally assessed with new perspectives to inspire discoveries and applications.In this review,we focus on both classical and the latest findings related to NOTCH signaling to illustrate the history,architecture,regulatory mechanisms,contributions to physiological development,related diseases,and therapeutic applications of the NOTCH pathway.The contributions of NOTCH signaling to the tumor immune microenvironment and cancer immunotherapy are also highlighted.We hope this review will help not only beginners but also experts to systematically and thoroughly understand the NOTCH signaling pathway. | Binghan Zhou Wanling Lin Yaling Long Yunkai Yang Huan Zhang Kongming Wu Qian Chu | 2022 | Signal Transduction and Targeted Therapy2022，7，4： | 14 |
| 12 | Role of Sonic Hedgehog signaling during progression from inflammation to cancer in the stomach显示文摘Despite advances in treatment and the declining incidence,gastric cancer remains the second leading cause of cancer-related deaths in the world.Understanding the progression from inflammation to cancer in the stomach is crucial in the development of novel therapies and strategies for treating this disease.Chronic inflammation of the stomach is typically caused by Helicobacter pylori(H.pylori)and resulting lesions may lead to gastric cancer.During the progression from inflammation to cancer,the stomach epithelium changes with evidence of the disruption of normal epithelial cell differentiation and infiltrating inflammatory cells.Coincident with the development of atrophic gastritis and metaplasia,is the loss of the gastric morphogen Sonic Hedgehog(Shh).Given its critical role as a regulator of gastric tissue homeostasis,the disruption of Shh expression during inflammation correlates with the loss of normal epithelial cell differentiation,but this has only recently been rigorously tested in vivo using a unique mouse model of targeted gastric Shh deletion.While pre-neoplastic lesions such as atrophic gastritis and in-testinal metaplasia are associated with the loss of Shh within the acid-secreting glands of the stomach,there is a clear link between elevated Shh and signaling to gastric cancers.The current review focuses on the effects of aberrant Shh expression and its role in the development of gastric cancer,specifically in response to H.pylori infection. | Alexander E Sherman Yana Zavros | 2011 | World Journal of Gastrointestinal Pathophysiology2011，2，6： | 14 |
| 13 | S100B protein in tissue development,repair and regeneration显示文摘The Ca 2+-binding protein of the EF-hand type,S100B,exerts both intracellular and extracellular regulatory activities.As an intracellular regulator,S100B is involved in the regulation of energy metabolism,transcription,protein phosphorylation,cell proliferation,survival,differentiation and motility,and Ca 2+ homeostasis,by interacting with a wide array of proteins(i.e.,enzymes,enzyme substrates,cytoskeletal subunits,scaffold/adaptor proteins,transcription factors,ubiquitin E3 ligases,ion channels) in a restricted number of cell types.As an extracellular signal,S100B engages the pattern recognition receptor,receptor for advanced glycation end-products(RAGE),on immune cells as well as on neuronal,astrocytic and microglial cells,vascular smooth muscle cells,skeletal myoblasts and cardiomyocytes.However,RAGE may not be the sole receptor activated by S100B,the protein being able to enhance bFGF-FGFR1 signaling by interacting with FGFR1-bound bFGF in particular cell types.Moreover,extracellular effects of S100B vary depending on its local concentration.Increasing evidence suggests that at the concentration found in extracellular fluids in normal physiological conditions and locally upon acute tissue injury,which is up to a few nM levels,S100B exerts trophic effects in the central and peripheral nervous system and in skeletal muscle tissue thus participating in tissue homeostasis.The present commentary summarizes results implicating intracellular and extracellular S100B in tissue development,repair and regeneration. | Guglielmo Sorci Francesca Riuzzi Cataldo Arcuri Claudia Tubaro Roberta Bianchi Ileana Giambanco Rosario Donato | 2013 | World Journal of Biological Chemistry2013，4，1： | 14 |
| 14 | Immune Homeostasis: Effects of Chinese Herbal Formulae and Herb-Derived Compounds on Allergic Asthma in Different Experimental Models显示文摘Allergic asthma is thought to arise from an imbalance of immune regulation, which is characterized by the production of large quantities of Ig E antibodies by B cells and a decrease of the interferon-γ/interleukin-4(Th1/Th2) ratio. Certain immunomodulatory components and Chinese herbal formulae have been used in traditional herbal medicine for thousands of years. However, there are few studies performing evidence-based Chinese medicine(CM) research on the mechanisms and efficacy of these drugs in allergic asthma. This review aims to explore the roles of Chinese herbal formulae and herb-derived compounds in experimental research models of allergic asthma. We screened published modern CM research results on the experimental effects of Chinese herbal formulae and herb-derived bioactive compounds for allergic asthma and their possible underlying mechanisms in English language articles from the Pub Med and the Google Scholar databases with the keywords allergic asthma, experimental model and Chinese herbal medicine. We found 22 Chinese herb species and 31 herb-derived anti-asthmatic compounds as well as 12 Chinese herbal formulae which showed a reduction of airway hyperresponsiveness, allergen-specific immunoglobulin E, inflammatory cell infiltration and a regulation of Th1 and Th2 cytokines in vivo, in vitro and ex vivo, respectively. Chinese herbal formulae and herbderived bioactive compounds exhibit immunomodulatory, anti-inflammatory and anti-asthma activities in different experimental models and their various mechanisms of action are being investigated in modern CM research with genomics, proteomics and metabolomics technologies, which will lead to a new era in the development of new drug discovery for allergic asthma in CM. | LIU Lu WANG Lin-peng HE Shan MA Yan | 2018 | Chinese Journal of Integrative Medicine2018，24，5： | 14 |
| 15 | Two RING-Finger Ubiquitin E3 Ligases Regulate the Degradation of SPX4, An Internal Phosphate Sensor, for Phosphate Homeostasis and Signaling in Rice显示文摘SPX-domain-containing proteins (SPXs) play an important role in inorganic phosphate (Pi) sensing,signaling,and transport in eukaryotes.In plants,SPXs are known to integrate cellular Pi status and negatively regulate the activity of Pi central regulators,the PHOSPATE STARVATION RESPONSE proteins (PHRs).The stability of SPXs,such as SPX4,is reduced under Pi-deficient conditions.However,the mechanisms by which SPXs are degraded remain unclear.In this study,using a yeast-twhybrid screen we iden.tified two RING-finger ubiquitin E3 ligases regulating SPX4 degradation,designated SDEL1 and SDEL2,which were post-transcriptionally induced by Pi starvation.We found that both SDELs were located in the nucleus and cytoplasm,had ubiquitin E3 ligase activity,and directly ubiquitinated the K^213 and K^299 lysine residues in SPX4 to regulate its stability.Furthermore,we found that PHR2,a Pi central regulator in rice,could compete with SDELs by interacting with SPX4 under Pi-sufficient conditions,which protected SPX4 from ubiquitination and degradation.Consistent with the biochemical function of SDEL1 and SDEL2,overexpression of SDEL1 or SDEL2 resulted in Pi overaccumulation and induced Pi-starvation signaling even under Pi-sufficient conditions.Conversely,their loss-of-function mutants displayed decreased Pi accumulation and reduced Pi-starvation signaling.Collectively,our study revealed that SDEL1 and SDEL2 facilitate the degradation of SPX4 to modulate PHR2 activity and regulate Pi homeostasis and Pi signaling in response to external Pi availability in rice. | Wenyuan Ruan Meina Guo Xueqing Wang Zhenhui Guo Zhuang Xu Lei Xu Hongyu Zhao Haiji Sun Chengqi Yan Keke Yi | 2019 | Molecular Plant2019，12，8： | 14 |
| 16 | Mechanisms underlying the impaired contractility of diabetic cardiomyopathy显示文摘Cardiac dysfunction is a well-known consequence of diabetes,with sustained hyperglycaemia leading to the development of a cardiomyopathy that is independent of cardiovascular disease or hypertension.Animal models of diabetes are commonly used to study the pathophysiology of diabetic cardiomyopathy,with the hope that increased knowledge will lead ultimately to better therapeutic strategies being developed.At physiological temperature,left ventricular trabeculae isolated from the streptozotocin rat model of type 1 diabetes showed decreased stress and prolonged relaxation,but with no evidence that decreased contractility was a result of altered myocardial Ca2+handling.Although sarcoplasmic reticulum(SR)Ca2+reuptake appeared slower in diabetic trabeculae,it was offset by an increase in actionpotential duration,thereby maintaining SR Ca2+content and favouring increased contraction force.Frequency analysis of t-tubule distribution by confocal imaging of ventricular tissue labeled with wheat germ agglutinin or ryanodine receptor antibodies showed a reduced T-power for diabetic tissue,but the differences were minor in comparison to other models of heart failure.The contractile dysfunction appeared to be the result of disrupted F-actin in conjunction with the increased typeⅠcollagen,with decreased myofilament Ca2+sensitivity contributing to the slowed relaxation. | Marie-Louise Ward David J Crossman | 2014 | World Journal of Cardiology2014，6，7： | 13 |
| 17 | Exosomes-the enigmatic regulators of bone homeostasis显示文摘Exosomes are a heterogeneous group of cell-derived membranous structures, which mediate crosstalk interaction between cells.Recent studies have revealed a close relationship between exosomes and bone homeostasis. It is suggested that bone cells can spontaneously secret exosomes containing proteins, lipids and nucleic acids, which then to regulate osteoclastogenesis and osteogenesis. However, the network of regulatory activities of exosomes in bone homeostasis as well as their therapeutic potential in bone injury remain largely unknown. This review will detail and discuss the characteristics of exosomes, the regulatory activities of exosomes in bone homeostasis as well as the clinical potential of exosomes in bone injury. | Minhao Gao Weiyang Gao J. M. Papadimitriou Changqing Zhang Junjie Gao Minghao Zheng | 2018 | Bone Research2018，6，4： | 13 |
| 18 | Vitamin D deficiency in chronic liver disease显示文摘Vitamin D is an important secosteroid hormone with known effect on calcium homeostasis,but recently there is increasing recognition that vitamin D also is involved in cell proliferation and differentiation,has immunomodulatory and anti-inflammatory properties.Vitamin D deficiency has been frequently reported in many causes of chronic liver disease and has been associated with the development and evolution of non-alcoholic fatty liver disease(NAFLD)and chronic hepatitis C(CHC)virus infection.The role of vitamin D in the pathogenesis of NAFLD and CHC is not completely known,but it seems that the involvement of vitamin D in the activation and regulation of both innate and adaptive immune systems and its antiproliferative effect may explain its importance in these liver diseases.Published studies provide evidence for routine screening for hypovitaminosis D in patients with liver disease.Further prospectives studies demonstrating the impact of vitamin D replacement in NAFLD and CHC are required. | Paula Iruzubieta lvaro Terán Javier Crespo Emilio Fábrega | 2014 | World Journal of Hepatology2014，6，12： | 13 |
| 19 | Chlorogenic Acid Maintains Glucose Homeostasis through Modulating the Expression of SGLT-1,GLUT-2,and PLG in Different Intestinal Segments of Sprague-Dawley Rats Fed a High-Fat Diet显示文摘Objective To reveal the effects and related mechanisms of chlorogenic acid(CGA)on intestinal glucose homeostasis.Methods Forty male Sprague-Dawley rats were randomly and equally divided into four groups:normal chow(NC),high-fat diet(HFD),HFD with low-dose CGA(20 mg/kg,HFD-LC),and HFD with high-dose CGA(90 mg/kg,HFD-HC).The oral glucose tolerance test was performed,and fast serum insulin(FSI)was detected using an enzyme-linked immunosorbent assay.The m RNA expression levels of glucose transporters(Sglt-1 and Glut-2)and proglucagon(Plg)in different intestinal segments(the duodenum,jejunum,ileum,and colon)were analyzed using quantitative real-time polymerase chain reaction.SGLT-1 protein and the morphology of epithelial cells in the duodenum and jejunum was localized by using immunofluorescence.Results At both doses,CGA ameliorated the HFD-induced body weight gain,maintained FSI,and increased postprandial 30-min glucagon-like peptide 1 secretion.High-dose CGA inhibited the HFD-induced elevation in Sglt-1 expression.Both CGA doses normalized the HFD-induced downregulation of Glut-2 and elevated the expression of Plg in all four intestinal segments.Conclusion An HFD can cause a glucose metabolism disorder in the rat intestine and affect body glucose homeostasis.CGA can modify intestinal glucose metabolism by regulating the expression of intestinal glucose transporters and Plg,thereby controlling the levels of blood glucose and insulin to maintain glucose homeostasis. | PENG Bing Jie ZHU Qi ZHONG Ying Li XU Shi Hao WANG Zheng | 2015 | Biomedical and Environmental Sciences2015，28，12： | 12 |
| 20 | Limbal stem cells: Central concepts of corneal epithelial homeostasis显示文摘A strong cohort of evidence exists that supports the localisation of corneal stem cells at the limbus. The distinguishing characteristics of limbal cells as stem cells include slow cycling properties, high proliferative potential when required, clonogenicity, absence of differentiation marker expression coupled with positive expression of progenitor markers, multipotency, centripetal migration, requirement for a distinct niche environment and the ability of transplanted limbal cells to regenerate the entire corneal epithelium. The existence of limbal stem cells supports the prevailing theory of corneal homeostasis, known as the XYZ hypothesis where X represents proliferation and stratification of limbal basal cells, Y centripetal migration of basal cells and Z desquamation of superficial cells. To maintain the mass of cornea, the sum of X and Y must equal Z and very elegant cell tracking experiments provide strong evidence in support of this theory. However, several recent stud-ies have suggested the existence of oligopotent stem cells capable of corneal maintenance outside of the limbus. This review presents a summary of data which led to the current concepts of corneal epithelial homeostasis and discusses areas of controversy surrounding the existence of a secondary stem cell reservoir on the corneal | Jinny J Yoon Salim Ismail Trevor Sherwin | 2014 | World Journal of Stem Cells2014，6，4： | 11 |
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