Evidence map›Paper›PMID 30227272›Full record

ReviewFree radical biology & medicine2018

Targeting mitochondrial dysfunction and oxidative stress in heart failure: Challenges and opportunities.

Ligia Akemi Kiyuna, Rudá Prestes E Albuquerque, Che-Hong Chen, Daria Mochly-Rosen, Julio Cesar Batista Ferreira

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
7.4field-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

124 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

64 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

5 authors at 2 institutions in 3 countries.

Ligia Akemi KiyunaDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil.
Rudá Prestes E AlbuquerqueDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil.
Che-Hong ChenDepartment of Chemical and Systems Biology, Stanford University School of Medicine, USA.
Daria Mochly-RosenDepartment of Chemical and Systems Biology, Stanford University School of Medicine, USA.
Julio Cesar Batista FerreiraDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil. Electronic address: jcesarbf@usp.br.
Universidade de São Paulo · BRStanford University · US

Funding

MECHANISMS OF ETHANOL-INDUCED CARDIAC PROTECTIONR01AA011147 · NIAAA · STANFORD UNIVERSITY · PI DARIA MOCHLY-ROSEN · 1996 to 2026
$8.2M
Mechanisms of Ethanol-Induced Cardiac ProtectionR37AA011147 · NIAAA · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 2009 to 2018
$5.3M
NIAAA NIH HHS R01 AA011147NIAAA NIH HHS R37 AA011147
6 · The paper itself

Abstract

Mitochondrial dysfunction characterized by impaired bioenergetics, oxidative stress and aldehydic load is a hallmark of heart failure. Recently, different research groups have provided evidence that selective activation of mitochondrial detoxifying systems that counteract excessive accumulation of ROS, RNS and reactive aldehydes is sufficient to stop cardiac degeneration upon chronic stress, such as heart failure. Therefore, pharmacological and non-pharmacological approaches targeting mitochondria detoxification may play a critical role in the prevention or treatment of heart failure. In this review we discuss the most recent findings on the central role of mitochondrial dysfunction, oxidative stress and aldehydic load in heart failure, highlighting the most recent preclinical and clinical studies using mitochondria-targeted molecules and exercise training as effective tools against heart failure.

Indexed as

AldehydesAnimalsAntioxidantsBiomimetic MaterialsCardiotonic AgentsClinical Trials as TopicDisease Models, AnimalDrug Evaluation, PreclinicalEnergy MetabolismExerciseHeart FailureHumansMalondialdehydeMitochondria, HeartOxidative StressReactive Nitrogen Species4-hydroxy-2-nonenalAldehydesAntioxidantsCardiotonic Agentscoenzyme Q10MalondialdehydeReactive Nitrogen SpeciesReactive Oxygen SpeciesSuperoxide DismutaseUbiquinoneAldehydesCardiovascular diseasesExercise trainingMitochondriaRedox imbalanceTherapy

Identifiers

PMID30227272
PMCPMC6309415
OpenAlexW2891777339

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.