The accumulation of senescent cells is an important contribution to degenerative aging; the inflammatory secretions of senescent cells actively degrade tissue structure and function. Animal studies have shown that selective destruction of senescent cells produces a meaningful degree of rejuvenation in old animals, alongside reversal of the pathology and progression of many age-related conditions. Senescent cells exhibit a sizable number of metabolic differences from normal cells, and researchers continue to explore these differences in search of novel ways to selectively destroy senescent cells. Here find an example of a novel finding, in which researchers explore the increased glycolysis that supports senescent cell energy metabolism and find a way to sabotage it.
Aging is a complex biological process, which is affected by several factors, lifestyle, diet, genetic or epigenetic factors, environmental stress, and metabolisms. Among others, several reports observed increased glycolysis in senescent cells (SnCs) and individual aging, whose causal effects or biological mechanisms have been unclear. Recently, we identified phosphoglycerate mutase 1 (PGAM1)-checkpoint kinase 1 (Chk1) binding as a booster for glycolytic metabolism and cell viability in SnCs.
Secretory phenotype of inflammatory factors, known as senescence associated secretory phenotype (SASP), is one of prominent properties in SnCs, which accelerates chronic inflammation and aging-relevant dysfunctions in tissues. Inhibition of PGAM1-Chk1 binding removes SnCs and suppresses SASP, alleviating organ damage and pulmonary fibrosis in vivo. Thus, PGAM1-Chk1 interaction represents a target for senolysis to preserve resilience in aging.
Link: https://doi.org/10.70401/Geromedicine.2026.0034
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