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| 1 | Driving neural regeneration through the mammalian target of rapamycin显示文摘Neurodegenerative disorders affect more than 30 million individuals throughout the world and lead to significant disability as well as death.These statistics will increase almost exponentially as the lifespan and age of individuals increase globally and individuals become more susceptible to acute disorders such as stroke as well as chronic diseases that involve cognitive loss,Alzheimer’s disease,and Parkinson’s disease.Current therapies for such disorders are effective only for a small subset of individuals or provide symptomatic relief but do not alter disease progression.One exciting therapeutic approach that may turn the tide for addressing neurodegenerative disorders involves the mammalian target of rapamycin(mTOR).mTOR is a component of the protein complexes mTOR Complex 1(mTORC1)and mTOR Complex 2(mTORC2)that are ubiquitous throughout the body and control multiple functions such as gene transcription,metabolism,cell survival,and cell senescence.mTOR through its relationship with phosphoinositide 3-kinas e(PI 3-K)and protein kinase B(Akt)and multiple downstream signaling pathways such as p70ribosomal S6 kinase(p70S6K)and proline rich Akt substrate 40 kDa(PRAS40)promotes neuronal cell regeneration through stem cell renewal and oversees critical pathways such as apoptosis,autophagy,and necroptosis to foster protection against neurodegenerative disorders.Targeting by mTOR of specific pathways that drive long-term potentiation,synaptic plasticity,andβ-amyl oid toxicity may offer new strategies for disorders such as stroke and Alzheimer’s disease.Overall,mTOR is an essential neuroprotective pathway but must be carefully targeted to maximize clinical efficacy and eliminate any clinical toxic side effects. | Kenneth Maiese | 2014 | Neural Regeneration Research2014，9，15： | 13 |
| 2 | Novel nervous and multi-system regenerative therapeutic strategies for diabetes mellitus with mTOR显示文摘Throughout the globe,diabetes mellitus(DM) is increasing in incidence with limited therapies presently available to prevent or resolve the significant complications of this disorder.DM impacts multiple organs and affects all components of the central and peripheral nervous systems that can range from dementia to diabetic neuropathy.The mechanistic target of rapamycin(m TOR) is a promising agent for the development of novel regenerative strategies for the treatment of DM.m TOR and its related signaling pathways impact multiple metabolic parameters that include cellular metabolic homeostasis,insulin resistance,insulin secretion,stem cell proliferation and differentiation,pancreatic β-cell function,and programmed cell death with apoptosis and autophagy.m TOR is central element for the protein complexes m TOR Complex 1(m TORC1) and m TOR Complex 2(m TORC2) and is a critical component for a number of signaling pathways that involve phosphoinositide 3-kinase(PI 3-K),protein kinase B(Akt),AMP activated protein kinase(AMPK),silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae)(SIRT1),Wnt1 inducible signaling pathway protein 1(WISP1),and growth factors.As a result,m TOR represents an exciting target to offer new clinical avenues for the treatment of DM and the complications of this disease.Future studies directed to elucidate the delicate balance m TOR holds over cellular metabolism and the impact of its broad signaling pathways should foster the translation of these targets into effective clinical regimens for DM. | Kenneth Maiese | 2016 | Neural Regeneration Research2016，11，3： | 13 |
| 3 | mTOR: Driving apoptosis and autophagy for neurocardiac complications of diabetes mellitus显示文摘The World Health Organization estimates that diabetes mellitus(DM) will become the seventh leading cause of death during the next two decades. DM affects approximately 350 million individuals worldwide and additional millions that remain undiagnosed are estimated to suffer from the complications of DM. Although the complications of DM can be seen throughout the body, the nervous, cardiac, and vascular systems can be significantly affected and lead to disorders that include cognitive loss, stroke, atherosclerosis, cardiac failure, and endothelial stem cell impairment. At the cellular level, oxidativestress is a significant determinant of cell fate during DM and leads to endoplasmic reticulum stress, mitochondrial dysfunction, apoptosis, and autophagy. Multiple strategies are being developed to combat the complications of DM, but it is the mechanistic target of rapamycin(mTOR) that is gaining interest in drug development circles especially for protective therapies that involve cytokines and growth factors such as erythropoietin. The pathways of mTOR linked to mTOR complex 1, mTOR complex 2, AMP activated protein kinase, and the hamartin(tuberous sclerosis 1)/tuberin(tuberous sclerosis 2) complex can ultimately influence neuronal, cardiac, and vascular cell survival during oxidant stress in DM through a fine interplay between apoptosis and autophagy. Further understanding of these mTOR regulated pathways should foster novel strategies for the complications of DM that impact millions of individuals with death and disability. | Kenneth Maiese | 2015 | World Journal of Diabetes2015，6，2： | 12 |
| 4 | SIRT1 and stem cells: In the forefront with cardiovascular disease, neurodegeneration and cancer显示文摘Cardiovascular disease, nervous system disorders, and cancer in association with other diseases such as diabetes mellitus result in greater than sixty percent of the global annual deaths. These noncommunicable diseases also affect at least one-third of the population in low and middle-income countries and lead to hypertension, elevated cholesterol, malignancy, and neurodegenerative disorders such as Alzheimer's disease and stroke. With the climbing lifespan of the world's population, increased prevalence of these disorders is expected requiring the development of new therapeutic strategies against these disabling disease entities. Targeting stem cellproliferation for cardiac disease, vascular disorders, cancer, and neurodegenerative disorders is receiving great enthusiasm, especially those that focus upon SIRT1, a mammalian homologue of the yeast silent information regulator-2. Modulation of the cellular activity of SIRT1 can involve oversight by nicotinamide/nicotinic acid mononucleotide adenylyltransferase, mammalian forkhead transcription factors, mechanistic of rapamycin pathways, and cysteine-rich protein 61, connective tissue growth factor, and nephroblastoma over-expressed gene family members that can impact cytoprotective outcomes. Ultimately, the ability of SIRT1 to control the programmed cell death pathways of apoptosis and autophagy can determine not only cardiac, vascular, and neuronal stem cell development and longevity, but also the onset of tumorigenesis and the resistance against chemotherapy. SIRT1 therefore has a critical role and holds exciting prospects for new therapeutic strategies that can offer reparative processes for cardiac, vascular, and nervous system degenerative disorders as well as targeted control of aberrant cell growth during cancer. | Kenneth Maiese | 2015 | World Journal of Stem Cells2015，7，2： | 10 |
| 5 | Targeting the core of neurodegeneration:FoxO,mTOR,and SIRT1显示文摘The global increase in lifespan noted not only in developed nations,but also in large developing countries parallels an observed increase in a significant number of noncommunicable diseases,most notable neurodegenerative disorders.Neurodegenerative disorders present a number of challenges for treatment options that do not resolve disease progression.Furthermore,it is believed by the year 2030,the services required to treat cognitive disorders in the United States alone will exceed$2 trillion annually.Mammalian forkhead transcription factors,silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae),the mechanistic target of rapamycin,and the pathways of autophagy and apoptosis offer exciting avenues to address these challenges by focusing upon core cellular mechanisms that may significantly impact nervous system disease.These pathways are intimately linked such as through cell signaling pathways involving protein kinase B and can foster,sometimes in conjunction with trophic factors,enhanced neuronal survival,reduction in toxic intracellular accumulations,and mitochondrial stability.Feedback mechanisms among these pathways also exist that can oversee reparative processes in the nervous system.However,mammalian forkhead transcription factors,silent mating type information regulation 2 homolog 1,mechanistic target of rapamycin,and autophagy can lead to cellular demise under some scenarios that may be dependent upon the precise cellular environment,warranting future studies to effectively translate these core pathways into successful clinical treatment strategies for neurodegenerative disorders. | Kenneth Maiese | 2021 | Neural Regeneration Research2021，16，3： | 6 |
| 6 | Erythropoietin and diabetes mellitus显示文摘Erythropoietin(EPO) is a 30.4 k Da growth factor and cytokine that governs cell proliferation, immune modulation, metabolic homeostasis, vascular function, and cytoprotection. EPO is under investigation for the treatment of variety of diseases, but appears especially suited for the treatment of disorders of metabolism that include diabetes mellitus(DM). DM and the com-plications of this disease impact a significant portion of the global population leading to disability and death with currently limited therapeutic options. In addition to its utility for the treatment of anemia, EPO can improve cardiac function, reduce fatigue, and improve cognition in patients with DM as well as regulate cellular energy metabolism, obesity, tissue repair and regeneration, apoptosis, and autophagy in experimental models of DM. Yet, EPO can have adverse effects that involve the vasculature system and unchecked cellular proliferation. Critical to the cytoprotective capacity and the potential for a positive clinical outcome with EPO are the control of signal transduction pathways that include protein kinase B, the mechanistic target of rapamycin, Wnt signaling, mammalian forkhead transcription factors of the O class, silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae), and AMP activated protein kinase. Therapeutic strategies that can specifically target and control EPO and its signaling pathways hold great promise for the development of new and effective clinical treatments for DM and the complications of this disorder. | Kenneth Maiese | 2015 | World Journal of Diabetes2015，6，14： | 6 |
| 7 | Novel applications of trophic factors,Wnt and WISP for neuronal repair and regeneration in metabolic disease显示文摘Diabetes mellitus affects almost 350 million individuals throughout the globe resulting in significant morbidity and mortality. Of further concern is the growing population of individuals that remain undiagnosed but are susceptible to the detrimental outcomes of this disorder. Diabetes mellitus leads to multiple complications in the central and peripheral nervous systems that include cognitive impairment, retinal disease, neuropsychiatric disease, cerebral ischemia, and peripheral nerve degeneration. Although multiple strategies are being considered, novel targeting of trophic factors, Wnt signaling, Wnt1 inducible signaling pathway protein 1, and stem cell tissue regeneration are considered to be exciting prospects to overcome the cellular mechanisms that lead to neuronal injury in diabetes mellitus involving oxidative stress, apoptosis, and autophagy. Pathways that involve insulin-like growth factor-1, fibroblast growth factor, epidermal growth factor, and erythropoietin can govern glucose homeostasis and are intimately tied to Wnt signaling that involves Wnt1 and Wnt1 inducible signaling pathway protein 1(CCN4) to foster control over stem cell proliferation, wound repair, cognitive decline, β-cell proliferation, vascular regeneration, and programmed cell death. Ultimately, cellular metabolism through Wnt signaling is driven by primary metabolic pathways of the mechanistic target of rapamycin and AMP activated protein kinase. These pathways offer precise biological control of cellular metabolism, but are exquisitely sensitive to the different components of Wnt signaling. As a result, unexpected clinical outcomes can ensue and therefore demand careful translation of the mechanisms that govern neural repair and regeneration in diabetes mellitus. | Kenneth Maiese | 2015 | Neural Regeneration Research2015，10，4： | 5 |
| 8 | Impacting dementia and cognitive loss with innovative strategies: mechanistic target of rapamycin, clock genes, circular non-coding ribonucleic acids, and Rho/Rock显示文摘A significant global impact from dementia:According to the World Health Organization(Dua et al.,2017),the current numbers for the prevalence and treatment costs for dementia worldwide are staggering.Almost 50 million individuals suffer from dementia.Dementia is now considered to be the 7^th leading cause of death.Currently,at least five percent of the world’s elderly population,equal to approximately 47 million individuals,have dementia.Moreover,at least sixty percent reside in low and middle income countries.Almost seventy-five percent of these new cases are to occur in these countries.The number of new cases each year throughout the globe is increasing at approximately 10 million per year.By the year 2030,82 million people are expected to have dementia and by the year 2050,152 million are expected to have the disease. | Kenneth Maiese | 2019 | Neural Regeneration Research2019，14，5： | 5 |
| 9 | Programming Apoptosis and Autophagy with Novel Approaches for Diabetes Mellitus显示文摘 | Kenneth Maiese | 2015 | Current Neurovascular Research2015，，2： | 2 |
| 10 | Microglial integrity is maintained by erythropoietin through integration of Akt and its substrates of glycogen synthase kinase-3beta, beta-catenin, and nuclear factor-kappaB显示文摘 | Li F Chong ZZ Maiese K | 2006 | Curr Neurovasc Res2006，3，3： | 1 |
| 11 | Effect of acute and chronic arecoline treatment on cerebralmetabolism and blood flow in the conscious rat显示文摘 | MAIESE K HOLLOWAY H H LARSON D M | 1994 | Brain Res1994，641，1： | 1 |
| 12 | Calicheamicins,a novel family of antitumor antibiotics:taxonomy,fermentation and biological properties显示文摘 | Maiese W M Lechevauer M P Lechevalier H A | 1989 | J Antibiot1989，42，4： | 1 |
| 13 | Erythropoietin on a tightrope: Balancing neuronal and vascular protection between intrinsic and extrinsic pathways显示文摘 | Li F Chong ZZ Maiese K | 2004 | Neurosignals2004，13，6： | 1 |
| 14 | Insights into oxidative stress and potentialnovel therapeutic targets for Alzheimer disease显示文摘 | Maiese K Chong ZZ | 2004 | Restor NeurolNeurosci2004，22，： | 1 |
| 15 | Erythropoietin is a novel vascular protectant through activation of Aktl and mitochondrialmodulation of cysteine proteases显示文摘 | CHONG Z Z KANG J MAIESE K | 2002 | Circulation2002，106，24： | 1 |
| 16 | Erythropoietin on a tightrope: Balan- cing neuronal and vascular protection between intrinsic and extrinsic pathways显示文摘 | Li F Chong ZZ Maiese K | 2004 | N eurosignals2004，13，6： | 1 |
| 17 | New strategies for Alzheimer dis-ease and cognitive impairment 显示文摘 | Maiese K Chang ZZ Hou J | 2009 | Oxid Med Cell Longev2009，2，5： | 1 |
| 18 | Erythropoietin is a novel vascular protectant through activation of AKT1 and mitochondrial modulation of cysteine proteases显示文摘 | Chong Z Z Kang J Q Maiese K | 2002 | Circulation2002，106，23： | 1 |
| 19 | Erythro- poietin is a novel vascular protectant through acti- vation of Aktl and mitochondrialmodulation of cys- teine proteases显示文摘 | CHONG Z Z KANG J MAIESE K | 2002 | Circulation2002，106，24： | 1 |
| 20 | Oxidative stress biology and cell injury during type 1 and type 2 diabetes mellitus显示文摘 | Maiese K Morhan SD Chong ZZ | 2007 | Curr Neurovasc Res2007，4，1： | 1 |
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