Given its state of stable proliferative inhibition, cellular senescence is primarily depicted as a critical mechanism by which organisms delay the progression of carcinogenesis. Cells undergoing senescence are often associated with the alteration of a series of specific features and functions, such as metabolic shifts, stemness induction, and microenvironment remodeling. However, recent research has revealed more complexity associated with senescence, including adverse effects on both physiological and pathological processes. How organisms evade these harmful consequences and survive has become an urgent research issue. Several therapeutic strategies targeting senescence, including senolytics, senomorphics, immunotherapy, and function restoration, have achieved initial success in certain scenarios. In this review, we describe in detail the characteristic changes associated with cellular senescence and summarize currently available countermeasures.
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http://dx.doi.org/10.1631/jzus.B2200178 | DOI Listing |
J Cell Physiol
January 2025
Department of Anesthesiology, University of Virginia, Charlottesville, Virginia, USA.
Carboxyl terminal modulator protein (CTMP) may be involved in various physiological and pathological processes, such as inflammation, tumor growth, and cardiac hypertrophy. Our recent study has shown that CTMP is increased with aging and plays a role in determining brain ischemic tolerance. However, it is not known how CTMP expression with aging is regulated and whether the changed CTMP expression has an effect on cell senescence.
View Article and Find Full Text PDFAging Cell
January 2025
Department of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Renal proximal tubular epithelial cell (PTEC) senescence and defective autophagy contribute to kidney aging, but the mechanisms remain unclear. Caveolin-1 (CAV1), a crucial component of cell membrane caveolae, regulates autophagy and is associated with cellular senescence. However, its specific role in kidney aging is poorly understood.
View Article and Find Full Text PDFJ Virol
January 2025
Institute for Medical Virology and Epidemiology of Viral Diseases, University Hospital Tübingen, Tübingen, Germany.
The human genome is like a museum of ancient retroviral infections. It contains a large number of endogenous retroviruses (ERVs) that bear witness to past integration events. About 5,000 of them are so-called long terminal repeat 12 (LTR12) elements.
View Article and Find Full Text PDFTransplantation
January 2025
Interdisciplinary Transplantation, Children's Hospital, Hannover Medical School, Hannover, Germany.
Cellular senescence has been identified as a potential driver of age-associated loss of organ function and as a mediator of age-related disease. Novel strategies in targeting senescent cells have shown promise in several organ systems to counteract functional decline, chronic inflammation, and age-dependent loss of repair capacity. Transgenic models have provided proof of principle that senolysis, the elimination of senescent cells, is an attractive strategy to overcome many age-related pathologies.
View Article and Find Full Text PDFNat Commun
January 2025
College of Pharmaceutical Sciences, National Key Laboratory of Advanced Drug Delivery and Release Systems, Zhejiang University, Hangzhou, China.
Nicotinamide (NAM), a main precursor of NAD+, is essential for cellular fuel respiration, energy production, and other cellular processes. Transporters for other precursors of NAD+ such as nicotinic acid and nicotinamide mononucleotide (NMN) have been identified, but the cellular transporter of nicotinamide has not been elucidated. Here, we demonstrate that equilibrative nucleoside transporter 1 and 2 (ENT1 and 2, encoded by SLC29A1 and 2) drive cellular nicotinamide uptake and establish nicotinamide metabolism homeostasis.
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