ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Thrombospondin-1 as a Mechanosensitive Matrix Protein Driving Fibroblast Senescence: A Novel Pathogenic Target for Pelvic Organ Prolapse.International urogynecology journal · 2026Article
- Review
- TSPO governs bone-lipid homeostasis by redirecting BMSC differentiation via the PI3K/AKT/β-catenin pathway.Stem cell research & therapy · 2026Article
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
- Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The cardiovascular system functions under continuous cyclic mechanical stretch, with disruptions in mechanical and biochemical signals contributing to disease progression. In cardiovascular disorders, these disruptions activate cardiac fibroblasts (CFs) and promote cellular senescence, yet it remains unclear whether mechanical stimuli alone can initiate this phenotype. Here, primary murine CFs are exposed to uniaxial stretch, and systematically varied mechanical parameters assessed their role in senescence induction. Loss of stretch magnitude and increase in frequency, mimicking a pathologic hypertrophy and fibrosis, led to a senescence phenotype, identified through cell cycle arrest, decreased lamin B expression, and DNA damage. Mechanically-induced CF senescence depends on p53/p21, whereas senescence triggered by oxidative stress or lamin A/C mutation proceeded via p16. Notably, mechanically-induced premature senescence is accompanied by reduced levels of the nuclear envelope protein emerin. These findings demonstrate that altered mechanical signals are sufficient to trigger premature senescence and implicate compromised nuclear integrity in the underlying mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.