Evidence map›Paper›PMID 34957264›Full record

ReviewFrontiers in cardiovascular medicine2021

Mitochondrial Metabolism in Myocardial Remodeling and Mechanical Unloading: Implications for Ischemic Heart Disease.

Min Jiang, Xiaoye Xie, Feng Cao, Yabin Wang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  4. Lactylation landscape of mitochondrial proteins in myocardial infarction.bioRxiv : the preprint server for biology · 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

4 authors at 3 institutions in 1 country.

Min JiangDepartment of Cardiology, National Clinical Research Center for Geriatric Disease, The Second Medical Center, Chinese People's Liberation Army General Hospital, Beijing, China.
Xiaoye XieDepartment of Cardiology, National Clinical Research Center for Geriatric Disease, The Second Medical Center, Chinese People's Liberation Army General Hospital, Beijing, China.
Feng CaoDepartment of Cardiology, National Clinical Research Center for Geriatric Disease, The Second Medical Center, Chinese People's Liberation Army General Hospital, Beijing, China.
Yabin WangDepartment of Cardiology, National Clinical Research Center for Geriatric Disease, The Second Medical Center, Chinese People's Liberation Army General Hospital, Beijing, China.
Chinese PLA General Hospital · CNChinese People's Liberation Army · CNPeople's Liberation Army No. 150 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic heart disease refers to myocardial degeneration, necrosis, and fibrosis caused by coronary artery disease. It can lead to severe left ventricular dysfunction (LVEF ≤ 35-40%) and is a major cause of heart failure (HF). In each contraction, myocardium is subjected to a variety of mechanical forces, such as stretch, afterload, and shear stress, and these mechanical stresses are clinically associated with myocardial remodeling and, eventually, cardiac outcomes. Mitochondria produce 90% of ATP in the heart and participate in metabolic pathways that regulate the balance of glucose and fatty acid oxidative phosphorylation. However, altered energetics and metabolic reprogramming are proved to aggravate HF development and progression by disturbing substrate utilization. This review briefly summarizes the current insights into the adaptations of cardiomyocytes to mechanical stimuli and underlying mechanisms in ischemic heart disease, with focusing on mitochondrial metabolism. We also discuss how mechanical circulatory support (MCS) alters myocardial energy metabolism and affects the detrimental metabolic adaptations of the dysfunctional myocardium.

Indexed as

heart failureischemic heart diseaseleft ventricular assist devicemechanical unloadingmitochondrial metabolismveno-arterial ECMO

Identifiers

PMID34957264
PMCPMC8695728
OpenAlexW4200110702

What Socratic 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 Socratic graph.