ArticleCell death & disease2024
The miR-30-5p/TIA-1 axis directs cellular senescence by regulating mitochondrial dynamics.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Stress granules and RNA-binding proteins in cellular senescence: a modular perspective on stress adaptation and inflammation.Molecular biology reports · 2026Review
- METTL3 Regulates the Senescence of Stem Cells From the Apical Papilla by Mediating the mInternational dental journal · 2026Article
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- TIA-1 promotes FUNDC1-mediated mitophagy to protect against stress-induced cellular senescence.Experimental & molecular medicine · 2026Article
- Mitochondrial quantity-quality imbalance in cellular senescence: practical readouts and minimal assay bundles.BMB reports · 2026Review
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Article
- Distinctive Gene Expression Profiles and Biological Responses of Skin Fibroblasts to Nicotinamide Mononucleotide: Implications for Longevity Effects on Skin.Biomedicines · 2025Article
- Extracellular vesicle-encapsulated microRNA signatures of cigarette smoking and smoking-related harm.Respiratory medicine · 2025Article
- Anti-senescence therapies: a new concept to address cardiovascular disease.Cardiovascular research · 2025Review
- Pterostilbene mitigates the senescence of human dermal fibroblast cells by enhancing mitochondrial quality.Frontiers in pharmacology · 2025Article
- Senescence, NK cells, and cancer: navigating the crossroads of aging and disease.Frontiers in immunology · 2025Review
- The Underestimated Role of Iron in Frontotemporal Dementia: A Narrative Review.International journal of molecular sciences · 2024Review
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Authors and funding
9 authors.
Funding
Abstract
Senescent cells exhibit a diverse spectrum of changes in their morphology, proliferative capacity, senescence-associated secretory phenotype (SASP) production, and mitochondrial homeostasis. These cells often manifest with elongated mitochondria, a hallmark of cellular senescence. However, the precise regulatory mechanisms orchestrating this phenomenon remain predominantly unexplored. In this study, we provide compelling evidence for decreases in TIA-1, a pivotal regulator of mitochondrial dynamics, in models of both replicative senescence and ionizing radiation (IR)-induced senescence. The downregulation of TIA-1 was determined to trigger mitochondrial elongation and enhance the expression of senescence-associated β-galactosidase, a marker of cellular senescence, in human foreskin fibroblast HS27 cells and human keratinocyte HaCaT cells. Conversely, the overexpression of TIA-1 mitigated IR-induced cellular senescence. Notably, we identified the miR-30-5p family as a novel factor regulating TIA-1 expression. Augmented expression of the miR-30-5p family was responsible for driving mitochondrial elongation and promoting cellular senescence in response to IR. Taken together, our findings underscore the significance of the miR-30-5p/TIA-1 axis in governing mitochondrial dynamics and cellular senescence.
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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 Socratic graph.