Evidence map›Paper›PMID 31658594›Full record

ReviewInternational journal of molecular sciences2019

TGF-β Signaling in Cellular Senescence and Aging-Related Pathology.

Kana Tominaga, Hiroshi I Suzuki

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 1 pooled it
16.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

242 citing papers in PubMed, 1 synthesis or guideline pooled it, 379 citations in OpenAlex.

  1. Pooled it
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  15. Repurposing niclosamide to mitigate inflammaging: a review of multi-target mechanisms in cellular senescence and age-related decline.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  16. Role of aging‑related cytokines in neurodegenerative disease (Review).International journal of molecular medicine · 2026
    Review
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182 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Kana TominagaDepartment of Biology and Paul F. Glenn Center for Biology of Aging Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. kanat@mit.edu.
Hiroshi I SuzukiDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. hisuzuki@mit.edu.ORCID 0000-0003-4682-5086
Massachusetts Institute of Technology · US

Funding

Grant-in-Aid for JSPS postdoc Fellows NAthe Osamu Hayaishi Memorial Scholarship for Study Abroad NA
6 · The paper itself

Abstract

Aging is broadly defined as the functional decline that occurs in all body systems. The accumulation of senescent cells is considered a hallmark of aging and thought to contribute to the aging pathologies. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that regulates a myriad of cellular processes and has important roles in embryonic development, physiological tissue homeostasis, and various pathological conditions. TGF-β exerts potent growth inhibitory activities in various cell types, and multiple growth regulatory mechanisms have reportedly been linked to the phenotypes of cellular senescence and stem cell aging in previous studies. In addition, accumulated evidence has indicated a multifaceted association between TGF-β signaling and aging-associated disorders, including Alzheimer's disease, muscle atrophy, and obesity. The findings regarding these diseases suggest that the impairment of TGF-β signaling in certain cell types and the upregulation of TGF-β ligands contribute to cell degeneration, tissue fibrosis, inflammation, decreased regeneration capacity, and metabolic malfunction. While the biological roles of TGF-β depend highly on cell types and cellular contexts, aging-associated changes are an important additional context which warrants further investigation to better understand the involvement in various diseases and develop therapeutic options. The present review summarizes the relationships between TGF-β signaling and cellular senescence, stem cell aging, and aging-related diseases.

Indexed as

AgingAlzheimer DiseaseCell ProliferationCellular SenescenceFibrosisHematopoietic Stem CellsHomeostasisInflammationLigandsMesenchymal Stem CellsMuscular AtrophyObesitySignal TransductionStem CellsTransforming Growth Factor betaLigandsTransforming Growth Factor betaagingcellular senescencestem celltransforming growth factor-β (TGF-β)

Identifiers

PMID31658594
PMCPMC6834140
OpenAlexW2979971613

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.