Evidence map›Paper›PMID 41955326›Full record

ReviewCirculation research2026

Two Routes for Removing Unhealthy Mitochondria: Degradation and Secretion.

Xi Fang, Åsa B Gustafsson

Abstract readReview
In one paragraph

Review in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

2 authors.

Xi FangDepartment of Medicine (X.F.), University of California San Diego, La Jolla.ORCID 0000-0001-7816-8821
Åsa B GustafssonSkaggs School of Pharmacy and Pharmaceutical Sciences (A.B.G.), University of California San Diego, La Jolla.ORCID 0000-0001-6347-8210

Funding

NEDD4 in right ventricular developmentR01HL158761 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FANG, XI · 2021 to 2025
$2.5M
Molecular mechanisms and treatment of cardiomyopathy in Barth SyndromeR01HL157115 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FANG, XI · 2021 to 2025
$2.0M
Autophagy and Megamitochondria in Cardiac Aging and Heart FailureR01HL157265 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2021 to 2024
$1.9M
NHLBI NIH HHS R01 HL157115NHLBI NIH HHS R01 HL157265NHLBI NIH HHS R01 HL158761
6 · The paper itself

Abstract

Mitochondria are highly dynamic, double-membraned organelles that generate the majority of ATP in cardiomyocytes while supporting cellular homeostasis and signal transduction. Accumulation of dysfunctional mitochondria can promote cardiomyocyte loss, impair contractile function, and ultimately lead to myocardial damage. To preserve mitochondrial integrity, cardiomyocytes rely on multilayered quality control mechanisms to remove defective mitochondria. Two major routes have emerged for this process: degradation, primarily via autophagy, and secretion via extracellular vesicles. This review summarizes the mechanisms of mitochondrial degradation and secretion in the heart and highlights their contributions to cardiac disease progression and potential as therapeutic targets.

Indexed as

AutophagyExtracellular VesiclesHeart DiseasesMitochondria, HeartMitophagyMyocytes, CardiacAnimalsHumansSignal Transductionextracellular vesicleshomeostasismitochondriamitophagymyocytes, cardiac

Identifiers

PMID41955326
PMCPMC13344491

What OpenQuestion holds

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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.