The global rise in life expectancy has led to an increasing prevalence of age-related diseases, including neurodegenerative disorders, cancer, type 2 diabete...

Senescence is an irreversible pause in the cell cycle that promotes biological aging and inflammation. Proliferating cells can obscure the biology of senescent cells in culture. Tousian et al. develop SenLect to selectively purify senescent cells, enabling deeper resolution of SASP signatures, metabolic shifts, and organelle remodeling during senescence.

Senomorphic microRNAs (miRNAs) are a class of small regulatory RNAs that selectively suppress the senescence-associated secretory phenotype (SASP) without el...

Cellular senescence is a stress-responsive cell fate characterized by stable growth arrest and acquisition of a proinflammatory senescence-associated secretory phenotype. Senescent cells accumulate with advancing age and contribute to dysfunction and disease across multiple organ systems. In skeletal muscle (SkM), emerging evidence indicates that senescence arises across diverse cell populations that collectively reshape the SkM niche. Through the SASP and altered intercellular signaling, senescent cells promote chronic inflammation, fibrosis, impaired regeneration, and metabolic dysfunction that contribute to SkM loss, SkM weakness, functional decline, and frailty. This review synthesizes current knowledge of the molecular drivers, hallmarks, and cellular origins of senescence within SkM and highlights the physiological consequences that extend from the cellular to the organismal level. We also discuss emerging senotherapeutic strategies that hold promise for optimizing SkM health and function with aging and disease.

Cellular senescence is a complex biological process characterized by irreversible cell-cycle arrest and acquisition of the senescence-associated secretory phenotype (SASP). Beyond biochemical stress,...

In Aging, researchers have described the differences between the secretions of cells driven senescent through a cancer gene and cells that stopped proliferating due to p16 expression. A difference of kind The SASP is a mix of many components that have various effects on the cells exposed to it. While inflammatory factors, such as cytokines

A new study links an age-related decline in cellular maintenance to impaired immune clearance. Activating the pathway reduced signs of senescence in aged mice [1]. Senescence and autophagy Cellular senescence, which occurs when cells stop dividing and start emitting largely pro-inflammatory stress signals, the senescence-associated secretory phenotype (SASP), is a double-edged sword. On the one

Background Current barriers to achieving radical life extension include the inability to use syngeneic, youthful mesenchymal stem cells (MSCs) and the anti-regenerative effects of senescence-associated secretory phenotype (SASP) factors. We aim to overcome this by a combination approach in which senescent cell burden is reduced utilizing SenoVax™ a dendritic cell based senolytic immunotherapy combined with syngeneic pluripotent stem cell derived MSC. Methods We induced hepatic injury and accelerated aging using two established murine models: carbon tetrachloride (CCl₄) mediated liver injury and doxorubicin induced systemic senescence. Animals were treated with control, SenoVax, pMSCs or the combination. Outcomes included biochemical and histologic indices of liver injury, circulating and tissue biomarkers of senescence (IL-11, YKL-40, IL-6, IL-23 R) and regeneration (Klotho, FGF-2, neo-VEGF, GDF-11), Results Both CCl₄ and doxorubicin induced a robust senescent phenotype characterized by increased pro-inflammatory and pro-fibrotic mediators and downregulation of regenerative biomarkers. Combined senolytic and pMSC therapy outperformed mono therapies and produced clear synergistic benefits, including significant biochemical improvement of liver failure parameters, reversal of accelerated aging features, and restoration of regenerative signaling pathways. Senolytic monotherapy yielded partial improvements, while pMSCs alone showed limited activity in the presence of a high senescent-cell burden. Conclusions These findings support a mechanistic model in which senescent cells and SASP factors directly suppress MSC-mediated tissue repair. Targeted senolytic immunotherapy enhances the efficacy of regenerative interventions and represents a promising combinatorial strategy for chronic disease management and potentially for modifying biological aging itself. Clinical trial number Not applicable.

A deep learning-based biomarker, SASP Score, evaluates the combined effects of the senescence-associated secretory phenotype circulating in the bloodstream.

Researchers have created a deep learning-based biomarker, SASP Score, that evaluates the combined effects of the senescence-associated secretory phenotype (SASP) circulating in the bloodstream. Measuring an overall burden Gathering the data needed to evaluate a person's circulating SASP is as simple as taking a blood draw. However, as bloodstream SASP is a combination of many