Aging is a dynamic, time-dependent process that is characterized by a gradual accumulation of cell damage. Continual functional decline in the intrinsic ability of living organisms to accurately regulate homeostasis leads to increased susceptibility and vulnerability to diseases. Many efforts have been put forth to understand and prevent the effects of aging. Thus, the major cellular and molecular hallmarks of aging have been identified, and their relationships to age-related diseases and malfunctions have been explored. Here, we use data from the CAS Content Collection to analyze the publication landscape of recent aging-related research. We review the advances in knowledge and delineate trends in research advancements on aging factors and attributes across time and geography. We also review the current concepts related to the major aging hallmarks on the molecular, cellular, and organismic level, age-associated diseases, with attention to brain aging and brain health, as well as the major biochemical processes associated with aging. Major age-related diseases have been outlined, and their correlations with the major aging features and attributes are explored. We hope this review will be helpful for apprehending the current knowledge in the field of aging mechanisms and progression, in an effort to further solve the remaining challenges and fulfill its potential.
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http://dx.doi.org/10.1021/acschemneuro.3c00531 | DOI Listing |
Biogerontology
January 2025
Centre for Global Health Research, Saveetha Medical College, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.
Aging is associated with a marked increase in cardiovascular diseases, such as myocardial infarction (MI). Cellular senescence is also a crucial factor in the development of age-related MI. Matrix metalloproteinases (MMPs) interaction with cellular senescence is a critical determinant of MI development and outcomes, most notably in the aged heart.
View Article and Find Full Text PDFInt Ophthalmol
January 2025
Department of Ophthalmology, The Second Hospital of Jilin University, #218 Ziqiang Street, Changchun, 130041, Jilin, China.
Purpose: The purpose of this study is to investigate the role of Secretogranin III (Scg3) in the pathogenesis of intraocular neovascular diseases and assess its potential as a therapeutic target for novel treatment strategies.
Methods: A literature review was conducted to examine the expression of Scg3 in intraocular neovascular diseases. We reviewed studies on the interaction of Scg3 with its homologous receptors and its effect on endothelial cell proliferation, migration, and vascular permeability-key processes involved in angiogenesis and neovascularization.
Biogerontology
January 2025
Center for Global Health Research, Saveetha Medical College, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.
The growing prevalence of age-related cardiovascular diseases (CVDs) poses significant health challenges, necessitating the formulation of novel treatment approaches. GATA4, a vital transcription factor identified for modulating cardiovascular biology and cellular senescence, is recognized for its critical involvement in CVD pathogenesis. This review collected relevant studies from PubMed, Google Scholar, and Science Direct using search terms like 'GATA4,' 'cellular senescence,' 'coronary artery diseases,' 'hypertension,' 'heart failure,' 'arrhythmias,' 'congenital heart diseases,' 'cardiomyopathy,' and 'cardiovascular disease.
View Article and Find Full Text PDFTher Adv Ophthalmol
January 2025
Department of Ophthalmology, Zealand University Hospital, Roskilde, Denmark.
Background: Age-related macular degeneration (AMD) is a prevalent cause of irreversible vision loss among the elderly. The prevalence and detailed characteristics of Charles Bonnet syndrome (CBS) remain largely unexplored in patients with geographic atrophy (GA) secondary to AMD.
Objectives: To investigate the prevalence and characteristics of CBS in patients with GA secondary to AMD.
Alzheimer's disease (AD) is an age-related neurodegenerative pathology. Brain-derived extracellular vesicles (EVs) have been demonstrated to be implicated in AD pathogenesis by facilitating the propagation of Tau, amyloid-β and inflammatory cytokines. However, the impact of peripheral EVs (pEVs) in AD pathogenesis remains poorly investigated.
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