Evidence map›Paper›PMID 40292006›Full record

ReviewFrontiers in physiology2025

Mechanisms underlying targeted mitochondrial therapy for programmed cardiac cell death.

Fengting Jing, Min Zhao, Hemin Xiong, Xin Zeng, Jun Jiang, Tao Li

Abstract readReview
In one paragraph

Review in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Aromatic amino acid metabolism shapes autophagy-mediated adaptation to iron deprivation in glioblastoma cells.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
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.

Fengting Jing *Key Laboratory of Medical Electrophysiology of Ministry of Education, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, China.
Min Zhao *Key Laboratory of Medical Electrophysiology of Ministry of Education, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, China.
Hemin XiongKey Laboratory of Medical Electrophysiology of Ministry of Education, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, China.
Xin ZengSchool of Continuing Education, Southwest Medical University, Luzhou, Sichuan, China.
Jun JiangDepartment of General Surgery (Thyroid Surgery), Southwest Medical University, Luzhou, Sichuan, China.
Tao LiKey Laboratory of Medical Electrophysiology of Ministry of Education, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart diseases are common clinical diseases, such as cardiac fibrosis, heart failure, hypertension and arrhythmia. Globally, the incidence rate and mortality of heart diseases are increasing by years. The main mechanism of heart disease is related to the cellular state. Mitochondrion is the organ of cellular energy supply, participating in various signal transduction pathways and playing a vital role in the occurrence and development of heart disease. This review summarizes the cell death patterns and molecular mechanisms associated with heart disease and mitochondrial dysfunction.

Indexed as

apoptosisautophagycardiomyocytecuproptosisferroptosismitochondriaPCDpyroptosis

Identifiers

PMID40292006
PMCPMC12021874

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.