Kunlin Jin, Ph.D.
Permanent URI for this communityhttps://hdl.handle.net/20.500.12503/21594
Professor, Pharmacology & Neuroscience
Member, Institute for Healthy Aging
Email: Kunlin.Jin@unthsc.edu
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Browsing Kunlin Jin, Ph.D. by Subject "aging"
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Item A Microcirculatory Theory of Aging(JKL International, 2019-06-01) Jin, KunlinAging is the progressive decline of physiological functions necessary for survival and reproduction. In gaining a better understanding of the inevitable aging process, the hope is to preserve, promote, or delay healthy aging through the treatment of common age-associated diseases. Although there are theories that try to explain the aging process, none of them seem to fully satisfy. Microcirculation describes blood flow through the capillaries in the circulatory system. The main functions of the microcirculation are the delivery of oxgen and nutrients and the removal of CO2, metabolic debris, and toxins. The microcirculatory impairment or dysfunction over time will result in the accumulation of toxic products and CO2 and loss of nutrition supplementation and O2 in corresponding tissue systems or internal organs, which eventually affect normal tissue and organ functions, leading to aging. Therefore, I propose a microcirculatory theory of aging: aging is the process of continuous impairment of microcirculation in the body.Item Aging During the Pandemic: Untangling the Complexities of COVID-19 and Geriatric Care(JKL International, 2023-05-16) Su, Kaimeng; Jin, KunlinThe COVID-19 pandemic has posed unprecedented challenges to the global healthcare system, with the elderly population being particularly vulnerable. This comprehensive review synthesizes the findings from publications in "Aging and Disease", highlighting the unique challenges older adults encountered during the pandemic and providing solutions thereof. These studies provide invaluable insights into the elderly population's vulnerabilities and needs during the COVID-19 pandemic. The susceptibility to the virus in older individuals remains debatable, and research on the clinical picture of COVID-19 in older populations has yielded insights into clinical features, molecular mechanisms, and potential therapeutic strategies. This review intends to shed light on the need of sustaining physical and mental well-being among older adults during the periods of lockdown by extensively exploring these concerns and emphasizing the need for targeted interventions and support systems for this population. Ultimately, the findings of these studies contribute to developing more effective and comprehensive approaches to managing and mitigating the risks posed by the pandemic to the elderly.Item AMPK Signaling Regulates the Age-Related Decline of Hippocampal Neurogenesis(JKL International, 2019-10-01) Wang, Brian Z.; Yang, Jane J.; Zhang, Hongxia; Smith, Charity A.; Jin, KunlinThe global incidence of age-associated neurological diseases is expected to rise with increasingly greying societies. In the aged brain, there is a dramatic decrease in the number of stem cells, which is a main cause for the decrease in brain function. Intrinsic factors, such as cell metabolism, have been studied but its role in neurogenesis is still unknown. Therefore, this study sought to establish whether AMP-activated protein kinase (AMPK) signaling does indeed regulate hippocampal neurogenesis in the aged brain. We found that i) AMPKalpha2 was the predominant catalytic subunit in the subgranular and subventricular zones; ii) AMPK activation was at a significantly higher level in the aged vs. young hippocampus; iii) short term (7 days) treatment with selective AMPK signaling inhibitor Compound C (10 mg/kg/day, i.p.) significantly increased the numbers of newborn (BrdU(+)), Type 2 (MCM2(+)), and Type 3 (DCX(+)) neural stem cells, but not Type 1 (GFAP(+)/Sox2(+)) cells, in the aged hippocampus. Taken together, our results demonstrate that AMPK signaling plays a critical role in the age-related decline of hippocampal neurogenesis.Item Combining Injectable Plasma Scaffold with Mesenchymal Stem/Stromal Cells for Repairing Infarct Cavity after Ischemic Stroke(JKL International, 2017-04-01) Zhang, Hongxia; Sun, Fen; Wang, Jixian; Xie, Luokun; Yang, Chenqi; Pan, Mengxiong; Shao, Bei; Yang, Guo-Yuan; Yang, Shaohua; Zhuge, Qichuan; Jin, KunlinStroke survivors are typically left with structural brain damage and associated functional impairment in the chronic phase of injury, for which few therapeutic options exist. We reported previously that transplantation of human embryonic stem cell (hESC)-derived neural stem cells together with Matrigel scaffolding into the brains of rats after focal ischemia reduced infarct volume and improved neurobehavioral performance. Matrigel is a gelatinous protein mixture extracted from mouse sarcoma cells, thus would not be approved for use as a scaffold clinically. In this study, we generated a gel-like scaffold from plasma that was controlled by changing the concentration of CaCl2. In vitro study confirmed that 10-20 mM CaCl2 and 10-40% plasma did not affect the viability and proliferation of human and rat bone marrow mesenchymal stem/stromal cells (BMSCs) and neural stem cells (NSCs). We transplanted plasma scaffold in combination of BMSCs into the cystic cavity after focal cerebral ischemia, and found that the atrophy volume was dramatically reduced and motor function was significantly improved in the group transplanted with scaffold/BMSCs compared with the groups treated with vehicle, scaffold or BMSCs only. Our data suggest that plasma-derived scaffold in combination of BMSCs is feasible for tissue engineering approach for the stroke treatment.Item Editorial: The NLRP3 inflammasome-mediated neuroinflammation and its related mitochondrial impairment in neurodegeneration(Frontiers Media S.A., 2023-01-31) Deng, Chao; Cai, Xiang; Wang, Qing; Jin, KunlinItem Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging(MDPI, 2021-03-16) Yu, Mengdi; Zhang, Hongxia; Wang, Brian; Zhang, Yinuo; Zheng, Xiaoying; Shao, Bei; Zhuge, Qichuan; Jin, KunlinAging is a fundamental biological process accompanied by a general decline in tissue function. Indeed, as the lifespan increases, age-related dysfunction, such as cognitive impairment or dementia, will become a growing public health issue. Aging is also a great risk factor for many age-related diseases. Nowadays, people want not only to live longer but also healthier. Therefore, there is a critical need in understanding the underlying cellular and molecular mechanisms regulating aging that will allow us to modify the aging process for healthy aging and alleviate age-related disease. Here, we reviewed the recent breakthroughs in the mechanistic understanding of biological aging, focusing on the adenosine monophosphate-activated kinase (AMPK), Sirtuin 1 (SIRT1) and mammalian target of rapamycin (mTOR) pathways, which are currently considered critical for aging. We also discussed how these proteins and pathways may potentially interact with each other to regulate aging. We further described how the knowledge of these pathways may lead to new interventions for antiaging and against age-related disease.Item Peripheral Circulating Exosomal miRNAs Potentially Contribute to the Regulation of Molecular Signaling Networks in Aging(MDPI, 2020-03-11) Zhang, Hongxia; Jin, KunlinPeople are living longer than ever. Consequently, they have a greater chance for developing a functional impairment or aging-related disease, such as a neurodegenerative disease, later in life. Thus, it is important to identify and understand mechanisms underlying aging as well as the potential for rejuvenation. Therefore, we used next-generation sequencing to identify differentially expressed microRNAs (miRNAs) in serum exosomes isolated from young (three-month-old) and old (22-month-old) rats and then used bioinformatics to explore candidate genes and aging-related pathways. We identified 2844 mRNAs and 68 miRNAs that were differentially expressed with age. TargetScan revealed that 19 of these miRNAs are predicated to target the 766 mRNAs. Pathways analysis revealed signaling components targeted by these miRNAs: mTOR, AMPK, eNOS, IGF, PTEN, p53, integrins, and growth hormone. In addition, the most frequently predicted target genes regulated by these miRNAs were EIF4EBP1, insulin receptor, PDK1, PTEN, paxillin, and IGF-1 receptor. These signaling pathways and target genes may play critical roles in regulating aging and lifespan, thereby validating our analysis. Understanding the causes of aging and the underlying mechanisms may lead to interventions that could reverse certain aging processes and slow development of aging-related diseases.