Evidence map›Paper›PMID 42150106›Full record

ArticleAging2026

Blue period - features of senescence 30 years after beta-galactosidase.

Chisaka Kuehnemann, Christopher D Wiley

Abstract read
In one paragraph

Article in Aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Chisaka KuehnemannJean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
Christopher D WileyJean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.

Funding

Tufts IRACDAK12GM133314 · NIGMS · TUFTS UNIVERSITY BOSTON · PI CLAIRE L MOORE, Jamie Lynn Maguire · 2019 to 2026
$8.4M
NIGMS NIH HHS K12 GM133314
6 · The paper itself

Abstract

Cellular senescence is a multi-phenotypic stress or damage response characterized by a stable cell cycle arrest and the secretion of a myriad of biologically active molecules, commonly known as the senescence-associated secretory phenotype (SASP). Thirty years ago, the identification of activated beta-galactosidase during senescence led to one of the first characterizations of senescent cell accumulation during biological aging. Since then, interventions that either selectively eliminate senescent cells or suppress the SASP have demonstrated that they are a major etiological agent for several degenerative pathologies associated with aging. As interest in the development of targeted therapeutics for senescence has grown, so too has the interest in the study of these cells. This has resulted in discovery of new features and phenotypes that often associate with senescence. Here, we review several of these key features of senescence, highlighting the strengths and caveats associated with each.

Indexed as

agingbiomarkerscell deathSASPsenescence

Identifiers

PMID42150106
PMCPMC13632857

What Socratic holds

Textmetadata
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 Socratic graph.