ArticleOxidative medicine and cellular longevity2021
Gasotransmitter CO Attenuates Bleomycin-Induced Fibroblast Senescence via Induction of Stress Granule Formation.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Stress granules and RNA-binding proteins in cellular senescence: a modular perspective on stress adaptation and inflammation.Molecular biology reports · 2026Review
- Partial Reprogramming in Senescent Schwann Cells Enhances Peripheral Nerve Regeneration via Restoration of Stress Granule Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Elucidating the Molecular Pathways and Therapeutic Interventions of Gaseous Mediators in the Context of Fibrosis.Antioxidants (Basel, Switzerland) · 2024Review
- CO-Induced TTP Activation Alleviates Cellular Senescence and Age-Dependent Hepatic SteatosisAging and disease · 2023Article
- GSPE Protects against Bleomycin-Induced Pulmonary Fibrosis in Mice via Ameliorating Epithelial Apoptosis through Inhibition of Oxidative Stress.Oxidative medicine and cellular longevity · 2022Article
- Deciphering the Active Compounds and Mechanisms of HSBDF for Treating ALIFrontiers in pharmacology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is recognized as a phenomenon wherein a proliferative cell undergoes a permanent growth arrest. The accumulation of senescent cells over time can become harmful and result in diseases and physiological decline. Plasminogen activator inhibitor (PAI-1) is considered as a critical marker and mediator of cellular senescence. The formation of stress granules (SGs) could prevent senescence through the sequestration of PAI-1, and we previously suggested that exogenous carbon monoxide (CO) could induce SG assembly via integrated stress response (ISR). Although CO is known to possess anti-inflammatory, antioxidative, and antiapoptotic properties, whether it exerts antisenescent effect is still not well defined. Here, to address whether CO-induced SGs could protect against cellular senescence, we first treated lung fibroblasts with bleomycin (BLM) to establish DNA damage-induced cellular senescence, and observed a significant increase of several hallmarks of senescence through SA-
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