Evidence map›Paper›PMID 36552277›Full record

ReviewBiology2022

A Unified Model of Age-Related Cardiovascular Disease.

Michael Fossel, Joe Bean, Nina Khera, Mikhail G Kolonin

Open access · goldAbstract readReview
In one paragraph

Review in Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Direct in vivo reprogramming to relieve tissue ischemia via induced vasculogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  5. Article
  6. Functional Features of Senescent Cells and Implications for Therapy.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Review
  9. Multiomics of Aging and Aging-Related Diseases.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Gene expression in mice with endothelium-specific telomerase knockout.Frontiers in cell and developmental biology · 2023
    Article
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 4 institutions in 1 country.

Michael FosselTelocyte, Grand Rapids, MI 49503, USA.ORCID 0000-0003-0726-2276
Joe BeanUniversity of Missouri School of Medicine, Kansas City, MO 65211, USA.
Nina KheraBuckingham Browne and Nichols School, Wellesley, MA 02138, USA.
Mikhail G KoloninUniversity of Texas Health Science Center at Houston, Houston, TX 77030, USA.ORCID 0000-0002-3743-7869
Buckingham Browne & Nichols · USEndocyte (United States) · USThe University of Texas Health Science Center at Houston · USUniversity of Missouri–Kansas City · US

Funding

Metabolic consequences of adipocyte progenitor replicative senescence: mechanism and interventionR01DK125922 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOLONIN, MIKHAIL G, MAHAN, KRISTIN ECKEL · 2021 to 2024
$1.5M
NIDDK NIH HHS R01 DK125922
6 · The paper itself

Abstract

Despite progress in biomedical technologies, cardiovascular disease remains the main cause of mortality. This is at least in part because current clinical interventions do not adequately take into account aging as a driver and are hence aimed at suboptimal targets. To achieve progress, consideration needs to be given to the role of cell aging in disease pathogenesis. We propose a model unifying the fundamental processes underlying most age-associated cardiovascular pathologies. According to this model, cell aging, leading to cell senescence, is responsible for tissue changes leading to age-related cardiovascular disease. This process, occurring due to telomerase inactivation and telomere attrition, affects all components of the cardiovascular system, including cardiomyocytes, vascular endothelial cells, smooth muscle cells, cardiac fibroblasts, and immune cells. The unified model offers insights into the relationship between upstream risk factors and downstream clinical outcomes and explains why interventions aimed at either of these components have limited success. Potential therapeutic approaches are considered based on this model. Because telomerase activity can prevent and reverse cell senescence, telomerase gene therapy is discussed as a promising intervention. Telomerase gene therapy and similar systems interventions based on the unified model are expected to be transformational in cardiovascular medicine.

Indexed as

agingautophagycardiovascular diseasecell senescencegene therapysenolyticssenotherapeuticstelomerasetelomere

Identifiers

PMID36552277
PMCPMC9775230
OpenAlexW4311719608

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.