Evidence map›Paper›PMID 33950478›Full record

ReviewHeart failure reviews2022

Mitochondrial abnormalities: a hub in metabolic syndrome-related cardiac dysfunction caused by oxidative stress.

Aoxue Li, Ningning Zheng, Xudong Ding

Open access · hybridAbstract readReview
In one paragraph

Review in Heart failure reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Oxidative Modifications in Cardiac Mitochondrial and CaHandbook of experimental pharmacology · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 3 institutions in 2 countries.

Aoxue Li *Department of Pharmaceutical Biotechnology, China Medical University-The Queen's University of Belfast Joint College, China Medical University, Liaoning, China.ORCID 0000-0003-1651-114X
Ningning Zheng *Department of Pathophysiology, College of Basic Medical Science, China Medical University, Liaoning, China.
Xudong DingDepartment of Anesthesiology, Shengjing Hospital, China Medical University, Liaoning, China. dingxd@sj-hospital.org.
China Medical University · CNJinzhou Medical University · CNNational Institutes of Pharmaceutical Research and Development (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome (MetS) refers to a group of cardiovascular risk elements comprising insulin resistance, obesity, dyslipidemia, increased glucose intolerance, and increased blood pressure. Individually, all the MetS components can lead to cardiac dysfunction, while their combination generates additional risks of morbidity and mortality. Growing evidence suggests that oxidative stress, a dominant event in cellular damage and impairment, plays an indispensable role in cardiac dysfunction in MetS. Oxidative stress can not only disrupt mitochondrial activity through inducing oxidative damage to mitochondrial DNA, RNA, lipids, and proteins but can also impair cardiomyocyte contractile function via mitochondria-related oxidative modifications of proteins central to excitation-contraction coupling. Furthermore, excessive reactive oxygen species (ROS) generation can lead to the activation of several mitochondria apoptotic signaling pathways, release of cytochrome c, and eventual induction of myocardial apoptosis. This review will focus on such processes of mitochondrial abnormalities in oxidative stress induced cardiac dysfunction in MetS.

Indexed as

Heart DiseasesMetabolic SyndromeHumansMitochondriaMyocardiumOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesCardiac dysfunctionMetabolic syndromeMitochondriaOxidative stressReactive oxygen species

Identifiers

PMID33950478
PMCPMC9197868
OpenAlexW3157459146

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.