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Stroke is a leading cause of disability and mortality all over the world. Due to an aging population, the incidence of stroke is rising significantly, which has led to devastating consequences for patients. In addition to traditional risk factors such as age, hypertension, hyperlipidemia, diabetes and atrial fibrillation, sleep disorders, as independent modifiable risk factors for stroke, have been highlighted increasingly. In this review, we provide an overview of common types of current sleep disturbances in cerebrovascular diseases, including insomnia, hypersomnia, breathing-related sleep disorders, and parasomnias. Moreover, evidence-based clinical therapeutic strategies and pitfalls of specific sleep disorders after stroke are discussed. We also review the neurobiological mechanisms of these treatments as well as their effects on stroke. Since depression after stroke is so prevalent and closely related to sleep disorders, treatments of post-stroke depression are also briefly mentioned in this review article.Ischemic heart disease (IHD) is defined as a syndrome of ischemic cardiomyopathy. Myogenesis and angiogenesis in the ischemic myocardium are important for cardiomyocyte (CM) survival, improving cardiac function and decreasing the progression of heart failure after IHD. Cellular senescence is a state of permanent irreversible cell cycle arrest caused by stress that results in a decline in cellular functions, such as proliferation, migration, homing, and differentiation. In addition, senescent cells produce the senescence-associated secretory phenotype (SASP), which affects the tissue microenvironment and surrounding cells by secreting proinflammatory cytokines, chemokines, growth factors, and extracellular matrix degradation proteins. The accumulation of cardiovascular-related senescent cells, including vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), CMs and progenitor cells, is an important risk factor of cardiovascular diseases, such as vascular aging, atherosclerotic plaque formation, myocardial infarction (MI) and ventricular remodeling. This review summarizes the processes of angiogenesis, myogenesis and cellular senescence after IHD. In addition, this review focuses on the relationship between cellular senescence and cardiovascular disease and the mechanism of cellular senescence. Finally, we discuss a potential therapeutic strategy for MI targeting senescent cells.Iron is an essential component in many biological processes in the human body. It is critical for the visual phototransduction cascade in the retina. However, excess iron can be toxic. selleck chemicals llc Iron accumulation and reduced efficiency of intracellular antioxidative defense systems predispose the aging retina to oxidative stress-induced cell death. Age-related macular degeneration (AMD) is characterized by retinal iron accumulation and lipid peroxidation. The mechanisms underlying AMD include oxidative stress-mediated death of retinal pigment epithelium (RPE) cells and subsequent death of retinal photoreceptors. Understanding the mechanism of the disruption of iron and redox homeostasis in the aging retina and AMD is crucial to decipher these mechanisms of cell death and AMD pathogenesis. The mechanisms of retinal cell death in AMD are an area of active investigation; previous studies have proposed several types of cell death as major mechanisms. Ferroptosis, a newly discovered programmed cell death pathway, has been associated with the pathogenesis of several neurodegenerative diseases. Ferroptosis is initiated by lipid peroxidation and is characterized by iron-dependent accumulation. In this review, we provide an overview of the mechanisms of iron accumulation and lipid peroxidation in the aging retina and AMD, with an emphasis on ferroptosis.Chronic kidney disease (CKD) is a growing problem among aging population, and the number of individuals at risk of end stage renal disease is rising. Part of the reason lies in incomplete understanding of the pathways underlying renal aging and kidney disease, as well as insufficient delivery of evidence-based treatment to elderly patients with CKD. This review aims to address these unsolved issues by delineating updated mechanisms of renal senescence and summarizing recent findings on key clinical aspects of CKD in the elderly. Challenges and obstacles in caring for older people with CKD are discussed, with an emphasis on modification of risk factors, prevention of acute kidney injury, stabilization of progression and decision on dialysis initiation.Action potential is transmitted to muscle fibers through specialized synaptic interfaces called neuromuscular junctions (NMJs). These structures are capped by terminal Schwann cells (tSCs), which play essential roles during formation and maintenance of the NMJ. tSCs are implicated in the correct communication between nerves and muscles, and in reinnervation upon injury. During aging, loss of muscle mass and strength (sarcopenia and dynapenia) are due, at least in part, to the progressive loss of contacts between muscle fibers and nerves. Despite the important role of tSCs in NMJ function, very little is known on their implication in the NMJ-aging process and in age-associated denervation. This review summarizes the current knowledge about the implication of tSCs in the age-associated degeneration of NMJs. We also speculate on the possible mechanisms underlying the observed phenotypes.Aging is a universal phenomenon in all biological organisms, defined by the loss of reproductive capacity and a progressive decline in fitness. In humans, aging is further associated with an increased incidence of disease conditions. The current aging population has become a primary public burden of the 21st century. Therefore, to delay the aging process and maintain fitness in the aging population, the discovery of novel anti-aging drugs remains an urgent need. In recent years, metformin, a widely used hypoglycemic drug, has attracted growing attention in the field of anti-aging research. Reportedly, numerous studies have indicated that metformin regulates aging-related pathways, possibly delaying the aging process by modulating these pathways. The elucidation of these anti-aging effects may provide insights into the age-retarding potential of metformin. The present review focuses on the predominant molecular mechanisms associated with aging, as well as the anti-aging effects of metformin.
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