Evidence map›Paper›PMID 40845481›Full record

ReviewJACC. Basic to translational science2025

Precision Medicine: Therapeutically Targeting Mitochondrial Alterations in Heart Failure.

Alex M Parker, Jarmon G Lees, Andrew J Murray, Anida Velagic, Shiang Y Lim, Miles J De Blasio, Rebecca H Ritchie

Abstract readReview
In one paragraph

Review in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 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

7 authors.

Alex M ParkerMonash Institute of Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia; St Vincent's Institute of Medical Research, Melbourne, Victoria, Australia.
Jarmon G LeesMonash Institute of Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia; St Vincent's Institute of Medical Research, Melbourne, Victoria, Australia; Department of Medicine and Surgery, University of Melbourne, Melbourne, Victoria, Australia.
Andrew J MurrayDepartment of Physiology, Development and Neuroscience, Cambridge, United Kingdom.
Anida VelagicMonash Institute of Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia.
Shiang Y LimMonash Institute of Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia; St Vincent's Institute of Medical Research, Melbourne, Victoria, Australia; Department of Medicine and Surgery, University of Melbourne, Melbourne, Victoria, Australia; National Heart Research Institute Singapore, National Heart Centre, Singapore.
Miles J De BlasioMonash Institute of Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia.
Rebecca H RitchieMonash Institute of Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia. Electronic address: Rebecca.Ritchie@monash.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A substantial component of the increasing global burden of cardiovascular disease is attributed to heart failure (HF), affecting over 64 million adults worldwide. Maladaptive mitochondrial respiratory alterations and oxidative stress are major contributors to HF development and progression, with subsequent downstream myocardial energetic impairment as a strong predictor of mortality. Current conventional therapeutic approaches, including renin-angiotensin-aldosterone system inhibition and β-adrenergic blockade, target neurohormonal aspects of HF and are effective in slowing disease progression. However, although these therapies may be associated with some improvement in myocardial energetics, they do not specifically address alterations in myocardial mitochondrial respiration or redox homeostasis. Targeting mitochondria has hence become a promising approach for more effective and tailored therapies. This review summarizes metabolic derangements that drive HF progression, with a specific focus on mitochondria. Importantly, here we address the essential knowledge gaps in the field, highlighting key translational strategies used to date, and the challenges associated with therapeutically targeting mitochondrial pathways, alongside recent developments seeking to deploy novel mitochondrial-targeted therapeutic approaches to treat HF.

Indexed as

cardiomyopathydrug discoverymyocardial metabolismoxidative stresspharmacotherapyrespiration

Identifiers

PMID40845481
PMCPMC12539467

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.