Evidence map›Paper›PMID 32043022›Full record

ReviewJACC. Basic to translational science2020

Targeting the Mitochondria in Heart Failure: A Translational Perspective.

Hani N Sabbah

Open access · goldAbstract readReview
In one paragraph

Review in JACC. Basic to translational science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
6.8field-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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Binaphthoquinone attenuates myofibroblast transition of human ventricular cardiac fibroblastsThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Electrostatic lipidopathy drives human diabetic heart failure.Cardiovascular diabetology. Endocrinology reports · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Tailored therapeutics for cardiomyopathies.Nature reviews. Cardiology · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

18 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.

Hani N SabbahDepartment of Medicine, Division of Cardiovascular Medicine, Henry Ford Hospital, Detroit, Michigan.
Henry Ford Hospital · US

Funding

Plasma Metabolomics and Myocardial Energetics in Heart FailureR01HL132154 · NHLBI · HENRY FORD HEALTH SYSTEM · PI LANFEAR, DAVID E, SABBAH, HANI N · 2017 to 2020
$3.1M
NHLBI NIH HHS R01 HL132154
6 · The paper itself

Abstract

The burden of heart failure (HF) in terms of health care expenditures, hospitalizations, and mortality is substantial and growing. The failing heart has been described as "energy-deprived" and mitochondrial dysfunction is a driving force associated with this energy supply-demand imbalance. Existing HF therapies provide symptomatic and longevity benefit by reducing cardiac workload through heart rate reduction and reduction of preload and afterload but do not address the underlying causes of abnormal myocardial energetic nor directly target mitochondrial abnormalities. Numerous studies in animal models of HF as well as myocardial tissue from explanted failed human hearts have shown that the failing heart manifests abnormalities of mitochondrial structure, dynamics, and function that lead to a marked increase in the formation of damaging reactive oxygen species and a marked reduction in on demand adenosine triphosphate synthesis. Correcting mitochondrial dysfunction therefore offers considerable potential as a new therapeutic approach to improve overall cardiac function, quality of life, and survival for patients with HF.

Indexed as

ADP, adenosine diphosphateATP, adenosine triphosphatecardiolipinCI (to V), complex I (to V)Drp, dynamin-related proteinETC, electron transport chainheart failureHF, heart failureHFpEF, heart failure with preserved ejection fractionHFrEF, heart failure with reduced ejection fractionLV, left ventricularMfn, mitofusinmitochondriaMPTP, mitochondrial permeability transition poremtDNA, mitochondrial deoxyribonucleic acidmyocardial energeticsOPA, optic atrophyoxidative phosphorylationPGC, peroxisome proliferator-activated receptor coactivatorPINK, phosphatase and tensin homolog–inducible kinaseROS, reactive oxygen speciesTAZ, tafazzin

Identifiers

PMID32043022
PMCPMC7000886
OpenAlexW3003721330

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.