Evidence map›Paper›PMID 41231357›Full record

ReviewCurrent heart failure reports2025

Endosomal Mechanisms in Heart Failure Pathophysiology.

Martijn F Hoes, Shujin Wang, Joost Jfp Luiken

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current heart failure reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Martijn F HoesDepartment of Cardiology, Maastricht University Medical Center+, Maastricht, the Netherlands.ORCID http://orcid.org/0000-0002-0234-438X
Shujin WangInstitute of Life Sciences, School of Basic Medicine, Chongqing Medical University, Chongqing, China.ORCID http://orcid.org/0009-0000-2278-8271
Joost Jfp LuikenDepartment of Cardiology, Maastricht University Medical Center+, Maastricht, the Netherlands. j.luiken@maastrichtuniversity.nl.ORCID http://orcid.org/0000-0002-8808-2631

Funding

Dutch Heart Foundation 2021T017National Natural Science Foundation of China 82100919
6 · The paper itself

Abstract

purpose of reviewTo examine the role of endosomal dysfunction in heart failure pathophysiology and evaluate its potential as a therapeutic target, particularly focusing on its regulation of cardiac metabolism. RECENT

findingsEndosomal dysfunction, driven by v-ATPase disassembly and loss of acidification, emerges as a key contributor to metabolic perturbations in heart failure. This dysfunction leads to uncontrolled CD36 translocation, resulting in lipotoxicity and inflammatory signaling through CD36-TLR4 complex formation. These mechanisms are especially relevant in diabetic cardiomyopathy and heart failure with preserved ejection fraction. The endosomal system represents a promising therapeutic target in heart failure, though its contribution varies among patients and disease stages. Recent advances in molecular imaging and biomarker analysis enable better patient stratification, opening new avenues for personalized endosome-targeted therapies in heart failure treatment.

Indexed as

Diabetic CardiomyopathiesEndosomesHeart FailureMyocardiumAnimalsCardiotonic AgentsCD36 AntigensDisease Models, AnimalHumansProtein TransportStroke VolumeVacuolar Proton-Translocating ATPasesCardiotonic AgentsCD36 AntigensVacuolar Proton-Translocating ATPasesCardiac metabolismCD36Endosomal functionv-ATPase

Identifiers

What OpenQuestion holds

Textmetadata
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.