Evidence map›Paper›PMID 36093152›Full record

ReviewFrontiers in cardiovascular medicine2022

Mitochondrial dysfunction in heart failure and its therapeutic implications.

Miaosen Liu, Jialan Lv, Zhicheng Pan, Dongfei Wang, Liding Zhao, Xiaogang Guo

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.5field-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

49 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
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  5. Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure.Journal of cardiovascular translational research · 2026
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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

6 authors at 2 institutions in 1 country.

Miaosen LiuClinical Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Jialan LvDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Zhicheng PanDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Dongfei WangDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Liding ZhaoDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiaogang GuoDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
First Affiliated Hospital Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ATP consumption in heart is very intensive to support muscle contraction and relaxation. Mitochondrion is the power plant of the cell. Mitochondrial dysfunction has long been believed as the primary mechanism responsible for the inability of energy generation and utilization in heart failure. In addition, emerging evidence has demonstrated that mitochondrial dysfunction also contributes to calcium dysregulation, oxidative stress, proteotoxic insults and cardiomyocyte death. These elements interact with each other to form a vicious circle in failing heart. The role of mitochondrial dysfunction in the pathogenesis of heart failure has attracted increasing attention. The complex signaling of mitochondrial quality control provides multiple targets for maintaining mitochondrial function. Design of therapeutic strategies targeting mitochondrial dysfunction holds promise for the prevention and treatment of heart failure.

Indexed as

calciumfusion and fissionheart failuremitochondriamitophagyreactive oxygen species

Identifiers

PMID36093152
PMCPMC9448986
OpenAlexW4292859831

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.