Evidence map›Paper›PMID 35853997›Full record

ReviewNature reviews. Cardiology2023

Mechanisms and consequences of endothelial cell senescence.

Samuel I Bloom, Md Torikul Islam, Lisa A Lesniewski, Anthony J Donato

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 299 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
299citing papers in PubMed, 1 pooled it
42.3field-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

299 citing papers in PubMed, 1 synthesis or guideline pooled it, 408 citations in OpenAlex.

  1. Pooled it
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  13. Life (Basel, Switzerland) · 2026
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239 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

4 authors at 1 institution in 1 country.

Samuel I Bloom *Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA.ORCID 0000-0003-1440-8122
Md Torikul Islam *Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA.
Lisa A LesniewskiDepartment of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA.
Anthony J DonatoDepartment of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA. anthonyjdonato@gmail.com.
University of Utah · US

Funding

IMPACT OF T CELLS ON AGE-RELATED VASCULAR DYSFUNCTION: A TRANSLATIONAL APPROACH - DIVERSITY SUPPLEMENTR01AG060395 · NIA · UNIVERSITY OF UTAH · PI DONATO, ANTHONY JOHN · 2019 to 2023
$2.5M
Integrative Mechanisms of Vascular AgingR01AG077751 · NIA · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Anthony John Donato, Lisa A Lesniewski · 2023 to 2026
$1.8M
Tissue senescence and age-associated metabolic dysfunction: the role of immune cell mediated inflammationR01AG076748 · NIA · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Lisa A Lesniewski · 2023 to 2026
$1.8M
Mechanisms of augmented atherosclerotic progression with agingR01AG048366 · NIA · UNIVERSITY OF UTAH · PI LESNIEWSKI, LISA A · 2016 to 2020
$1.7M
Telomere uncapping and arterial dysfunction: Novel mechanism and implications for agingR01AG050238 · NIA · UNIVERSITY OF UTAH · PI DONATO, ANTHONY JOHN · 2016 to 2020
$1.6M
Telomere uncapping as a novel mechanism for endothelial cell senescence and age-related arterial dysfunctionF31AG076312 · NIA · UNIVERSITY OF UTAH · PI BLOOM, SAMUEL · 2022 to 2023
$72k
Role of ARF6 in atherosclerotic burden and severityI01BX004492 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI LESNIEWSKI, LISA A · 2020 to 2023
–
BLRD VA I01 BX004492NIA NIH HHS F31 AG076312NIA NIH HHS R01 AG048366NIA NIH HHS R01 AG050238NIA NIH HHS R01 AG060395NIA NIH HHS R01 AG076748NIA NIH HHS R01 AG077751
6 · The paper itself

Abstract

Endothelial cells are located at the crucial interface between circulating blood and semi-solid tissues and have many important roles in maintaining systemic physiological function. The vascular endothelium is particularly susceptible to pathogenic stimuli that activate tumour suppressor pathways leading to cellular senescence. We now understand that senescent endothelial cells are highly active, secretory and pro-inflammatory, and have an aberrant morphological phenotype. Moreover, endothelial senescence has been identified as an important contributor to various cardiovascular and metabolic diseases. In this Review, we discuss the consequences of endothelial cell exposure to damaging stimuli (haemodynamic forces and circulating and endothelial-derived factors) and the cellular and molecular mechanisms that induce endothelial cell senescence. We also discuss how endothelial cell senescence causes arterial dysfunction and contributes to clinical cardiovascular diseases and metabolic disorders. Finally, we summarize the latest evidence on the effect of eliminating senescent endothelial cells (senolysis) and identify important remaining questions to be addressed in future studies.

Indexed as

Cardiovascular DiseasesEndothelial CellsCellular SenescenceEndothelium, VascularHumans

Identifiers

PMID35853997
PMCPMC10026597
OpenAlexW4285796211

What OpenQuestion holds

Textmetadata
LicenceTDM
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.