Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

TGF-β signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging

26 Jun 2018

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Genomics and Chromatin Dynamics
Share to MicroRNA in disease regulation
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 29967491
DOI: 10.1038/s41467-018-04994-z

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TGF-β signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac agingPMID 29967491Read ↗

TGF-β Signaling in Cellular Senescence and Aging-Related PathologySemantic proximity Read ↗

Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stabilitySemantic proximity Read ↗

Embryonic Stem Cell–Derived mmu-miR-291a-3p Inhibits Cellular Senescence in Human Dermal Fibroblasts Through the TGF-β Receptor 2 PathwaySemantic proximity Read ↗

ATOH8 binds SMAD3 to induce cellular senescence and prevent Ras-driven malignant transformationSemantic proximity Read ↗

New tricks for an old fox: Impact of TGFβ on the DNA damage response and genomic stabilitySemantic proximity Read ↗

KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin ReorganizationSemantic proximity Read ↗

SUV39H2/KMT1B Inhibits the cardiomyocyte senescence phenotype by down-regulating BTG2/PC3.Semantic proximity Read ↗

TGF-β/NF1/Smad4-mediated suppression of ANT2 contributes to oxidative stress in cellular senescence.Semantic proximity Read ↗

Cardiac myocyte miR-29 promotes pathological remodeling of the heart by activating Wnt signalingSemantic proximity Read ↗

Downregulation of long non-coding RNA H19 promotes P19CL6 cells proliferation and inhibits apoptosis during late-stage cardiac differentiation via miR-19b-modulated Sox6Semantic proximity Read ↗

MicroRNA ‐ 19a ‐ 3p Decreases with Age in Mice and Humans and Inhibits Osteoblast SenescenceSemantic proximity Read ↗

Histone H4K20 Trimethylation is Decreased in Murine Models of Heart DiseaseSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.