Evidence mapPaperPMID 41089829Full record

ReviewFrontiers in pharmacology2025

Mitochondrial dysfunction as a therapeutic nexus in HFpEF: therapeutic target and pharmacological advances.

Tian Yue, Dezhi Zheng, Jian He, Shiqiang Xiong, Junbo Xu, Jun Hou

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
field-weighted citation impact
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

8 citing papers in PubMed.

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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.

Tian Yue *Department of Cardiology, The Third People's Hospital of Chengdu/Affiliated Hospital of Southwest Jiaotong University, Chengdu Institute of Cardiovascular Disease, Chengdu, Sichuan, China.
Dezhi Zheng *Department of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan, Shandong, China.
Jian HeDepartment of Cardiology, The Third People's Hospital of Chengdu/Affiliated Hospital of Southwest Jiaotong University, Chengdu Institute of Cardiovascular Disease, Chengdu, Sichuan, China.
Shiqiang XiongDepartment of Cardiology, The Third People's Hospital of Chengdu/Affiliated Hospital of Southwest Jiaotong University, Chengdu Institute of Cardiovascular Disease, Chengdu, Sichuan, China.
Junbo XuDepartment of Cardiology, The Third People's Hospital of Chengdu/Affiliated Hospital of Southwest Jiaotong University, Chengdu Institute of Cardiovascular Disease, Chengdu, Sichuan, China.
Jun HouDepartment of Cardiology, The Third People's Hospital of Chengdu/Affiliated Hospital of Southwest Jiaotong University, Chengdu Institute of Cardiovascular Disease, Chengdu, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) with preserved ejection fraction (HFpEF) accounts for approximately 50% of all HF cases, and its incidence continues to rise with population aging and the surge in metabolic diseases. Unlike heart failure with reduced ejection fraction (HFrEF), HFpEF lacks effective therapeutic regimens to improve prognosis, with a 5-year mortality rate as high as 50%. Mitochondrial dysfunction, as a key link connecting metabolic disorders and abnormal myocardial systolic and diastolic function, has become a critical mechanism in the pathophysiology of HFpEF and a potential therapeutic target. This review systematically elaborates on the molecular mechanisms in HFpEF, such as mitochondrial energy metabolism disorders, dynamic imbalance, oxidative stress injury, and calcium signal dysregulation, comprehensively reviews the evidence for the effects of marketed drugs and drugs in clinical trials that improve mitochondrial function, and simultaneously explores emerging therapeutic strategies targeting mitochondria. This review aims to provide a theoretical reference for mechanistic research and drug development of HFpEF and promote the application of precision therapy targeting mitochondrial dysfunction in clinical practice.

Indexed as

drug developmentHFpEFmitochondrial dysfunctionmitochondrial targetingtherapeutic strategies

Identifiers

PMID41089829
PMCPMC12515642

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.