Evidence map›Paper›PMID 31689891›Full record

ReviewCells2019

The Role of Signaling Pathways of Inflammation and Oxidative Stress in Development of Senescence and Aging Phenotypes in Cardiovascular Disease.

John Papaconstantinou

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 3 pooled it
7.5field-weighted citation impact, top 2% 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

139 citing papers in PubMed, 3 syntheses or guidelines pooled it, 249 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. [Research progress on the pathogenesis and clinical treatment of cirrhotic cardiomyopathy].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis.International journal of molecular sciences · 2026
    Review
  14. Review
  15. Article
  16. Review
  17. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  18. Article
  19. Article
  20. Article

79 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

1 author at 1 institution in 1 country.

John Papaconstantinou5.138B Medical Research Building, 301 University Boulevard, Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, Galveston, TX 77555-0643, USA. jpapacon@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

UTMB OAIC Research Education Component (REC)P30AG024832 · NIA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI JAMES S. GOODWIN, MD, MELISSA M. MORROW · 2005 to 2026
$26.7M
OXIDATIVE STRESS,REPAIR OF OXIDIZED GUANINES IN AGED CELLSP01AG021830 · NIA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI PAPACONSTANTINOU, JOHN NMN · 2004 to 2010
$6.4M
NIA NIH HHS P01 AG021830NIA NIH HHS P30 AG024832
6 · The paper itself

Abstract

The ASK1-signalosome→p38 MAPK and SAPK/JNK signaling networks promote senescence (in vitro) and aging (in vivo, animal models and human cohorts) in response to oxidative stress and inflammation. These networks contribute to the promotion of age-associated cardiovascular diseases of oxidative stress and inflammation. Furthermore, their inhibition delays the onset of these cardiovascular diseases as well as senescence and aging. In this review we focus on whether the (a) ASK1-signalosome, a major center of distribution of reactive oxygen species (ROS)-mediated stress signals, plays a role in the promotion of cardiovascular diseases of oxidative stress and inflammation; (b) The ASK1-signalosome links ROS signals generated by dysfunctional mitochondrial electron transport chain complexes to the p38 MAPK stress response pathway; (c) the pathway contributes to the sensitivity and vulnerability of aged tissues to diseases of oxidative stress; and (d) the importance of inhibitors of these pathways to the development of cardioprotection and pharmaceutical interventions. We propose that the ASK1-signalosome regulates the progression of cardiovascular diseases. The resultant attenuation of the physiological characteristics of cardiomyopathies and aging by inhibition of the ASK1-signalosome network lends support to this conclusion. Importantly the ROS-mediated activation of the ASK1-signalosome p38 MAPK pathway suggests it is a major center of dissemination of the ROS signals that promote senescence, aging and cardiovascular diseases. Pharmacological intervention is, therefore, feasible through the continued identification of potent, non-toxic small molecule inhibitors of either ASK1 or p38 MAPK activity. This is a fruitful future approach to the attenuation of physiological aspects of mammalian cardiomyopathies and aging.

Indexed as

AgingAnimalsCardiovascular DiseasesCellular SenescenceHumansInflammationOxidative StressSignal TransductionagingASK1-signalosomecardiomyopathiesinflammationmitochondrial dysfunctionoxidative stressp38 MAPKsenescence

Identifiers

PMID31689891
PMCPMC6912541
OpenAlexW2988388473

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.