ArticleNature communications2018
TGF-β signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 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.
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Who cites it
109 citing papers in PubMed, 174 citations in OpenAlex.
- Growth factor applications and clinical translation: advances and challenges.Annals of medicine · 2026Review
- APC/C-CDH1 suppresses AROS-mediated protection against DNA damage-induced senescence by ubiquitination.BMB reports · 2026Article
- Non-Coding RNAs from Cardiac Development to Disease: Regulatory Context, Regenerative Potential, and Translational Limits.International journal of molecular sciences · 2026Review
- Circulating multi-omic signature of disease severity and cholangiocarcinoma in primary sclerosing cholangitis.Hepatology communications · 2026Article
- Role of Klhl14 in senescence and epithelial-to-mesenchymal transition via TGF-β modulation.Cell death & disease · 2026Article
- CK1-induced TERT phosphorylation mediates mitochondrial translocation to inhibit cardiomyocyte senescence and alleviate myocardial ischemia-reperfusion injury.Cell biology and toxicology · 2026Article
- Decoding noncoding RNAs in regulating cardiovascular aging and age-related conditions: the emerging landscape.Science China. Life sciences · 2026Review
- P38α MAPK-induced senescence in cranial suture progenitor cells promotes craniosynostosis.Communications biology · 2025Article
- Radiation-induced extracellular vesicles from cancer-associated fibroblasts drive oesophageal squamous cell carcinoma metastasis via the miR-193a-3p/PTEN/Akt pathway.Clinical and translational medicine · 2025Article
- S913 phosphorylation of Ulk1 protects the heart from aging through inhibition of cardiac senescence.Cardiovascular research · 2025Article
- Article
- Review
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- The value of miRNA-29b in the diagnosis of myocardial infarction and the evaluation of cardiac function after myocardial infarction.Cardiovascular diagnosis and therapy · 2025Article
- Histone Lactylation Antagonizes Senescence and Skeletal Muscle Aging by Modulating Aging-Related Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Development of a microRNA-Based age estimation model using whole-blood microRNA expression profiling.Non-coding RNA research · 2025Article
- ARID5A orchestrates cardiac aging and inflammation through MAVS mRNA stabilization.Nature cardiovascular research · 2025Article
- MicroRNA-29c-3p and -126a Contribute to the Decreased Angiogenic Potential of Aging Endothelial Progenitor Cells.International journal of molecular sciences · 2025Article
- Longevity mechanisms in cardiac aging: exploring calcium dysregulation and senescence.Biogerontology · 2025Review
- Review
49 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Cellular senescence is a well-orchestrated programmed process involved in age-related pathologies, tumor suppression and embryonic development. TGF-β/Smad is one of the predominant pathways that regulate damage-induced and developmentally programmed senescence. Here we show that canonical TGF-β signaling promotes senescence via miR-29-induced loss of H4K20me3. Mechanistically, oxidative stress triggers TGF-β signaling. Activated TGF-β signaling gives rise to acute accumulation of miR-29a and miR-29c, both of which directly suppress their novel target, Suv4-20h, thus reducing H4K20me3 abundance in a Smad-dependent manner, which compromises DNA damage repair and genome maintenance. Loss of H4K20me3 mediated by the senescent TGF-β/miR-29 pathway contributes to cardiac aging in vivo. Disruption of TGF-β signaling restores H4K20me3 and improves cardiac function in aged mice. Our study highlights the sequential mechanisms underlying the regulation of senescence, from senescence-inducing triggers to activation of responsive signaling followed by specific epigenetic alterations, shedding light on potential therapeutic interventions in cardiac aging.
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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.