Skip to content
Open access

Genotoxic and metabolic stress drive divergent senescence programs in human microglia

Sep 2026 · bioRxiv · 0 citations · 4 references
Biology

TL;DR

Investigating the impact of chronic genotoxic and metabolic stress on senescence-associated phenotypes in the human microglia cell line HMC3 demonstrated that chronic genotoxic and metabolic stress drive distinct yet overlapping senescence programs characterised by morphological changes, mitochondrial remodelling and persistent inflammatory activation.

Read PDF

Similar papers

Open access Sep 2026

Mitochondrial dysfunction and impaired osteogenic capacity define stress-induced osteoblast senescence

Cellular senescence has emerged as a key contributor to age-related skeletal deterioration; however, the defining characteristics of senescent osteoblasts remain incompletely understood, hindering efforts to identify the cellular mechanisms that drive age-associated bone loss and potential therapeutic targets. Here, we...

Tanja Frey, Hannah Vogg, Mubashir Ahmad et al. · 0 citations
Review Open access Aug 2026

Mitochondrial regulation of cellular senescence heterogeneity

Current understanding of mitochondrial regulation across senescence subtypes is synthesized and how mitochondrial dysfunction actively drives senescence heterogeneity is highlighted to provide a conceptual framework for developing precision interventions in aging and cancer.

Minseo Ahn, Sung-Jin Yoon, Jae Ho Seo · 0 citations
Open access Sep 2026

Lactate Receptor Activation Alleviates Senescence and Preserves Homeostasis of Aged Arteries

These findings identify age-associated loss of GPR81 as a driver of vascular metabolic dysfunction and cellular senescence and establish pharmacological GPR81 activation as a promising therapeutic strategy for preserving vascular homeostasis and mitigating age-associated cardiovascular disease.

Yu-Lun Wu, Hamsa Vardini Senthil Kumar, Sai Harsha Bhamidipati et al. · 0 citations
Review Open access Aug 2026

Pathogenic modulators of cellular senescence

Cellular senescence is characterized by irreversible cell-cycle arrest, with cells remaining viable and metabolically active. This state features a proinflammatory senescence-associated secretory phenotype (SASP) that can harm neighboring tissues. Accumulation of senescent cells accelerates age-related physiological de...

E. V. Simoroz, Y. V. Antonov, G. Muravyov et al. · 0 citations
Review Open access Sep 2026

Brain Aging and Cellular Senescence Trigger Neuroimmunological Dysregulation and Neurodegeneration

Cellular senescence during brain aging is a complex biological phenomenon triggered by age-related and external factors, leading to epigenetic and genetic alterations that impair cellular replication, cause mitochondrial dysfunction, and activate the senescence-associated secretory phenotype (SASP). This activation ini...

Vega-García Angélica, Manuel-Apolinar Leticia, Feria-Romero Iris Angélica et al. · 0 citations
Sep 2026

Aging-associated loss of CPEB4 impairs mitochondrial adaptation and promotes stress-induced senescence in alveolar type II cells.

Aging is associated with impaired lung repair and increased susceptibility to injury, yet the mechanisms underlying age-associated dysfunction of alveolar type II (AT2) cells remain poorly understood. Although cellular senescence is a hallmark of aging, emerging evidence suggests that aging is also characterized by pro...

Xin-Yi Li, Zhi-Fang Fu, Dan Sun et al. · 0 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.