Evidence map›Paper›PMID 36742465›Full record

ArticleThe journal of cardiovascular aging2023

The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure.

Benjamin Werbner, Omid Mohammad Tavakoli-Rouzbehani, Amir Nima Fatahian, Sihem Boudina

Open access · hybridAbstract read
In one paragraph

Article in The journal of cardiovascular aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% of its field
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  12. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  20. Mitochondria, Sex, and Cardiovascular Disease: A Complex Interplay.International journal of molecular sciences · 2025
    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

4 authors at 1 institution in 1 country.

Benjamin WerbnerDepartment of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT 84112, USA.ORCID 0000-0002-0450-659X
Omid Mohammad Tavakoli-RouzbehaniDepartment of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT 84112, USA.
Amir Nima FatahianDepartment of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT 84112, USA.
Sihem BoudinaDepartment of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT 84112, USA.ORCID 0000-0002-4711-1109
University of Utah · US

Funding

The Role of PRDM16 in Cardiac Development and CardiomyopathyR01HL149870 · NHLBI · UNIVERSITY OF UTAH · PI BOUDINA, SIHEM · 2020 to 2023
$2.8M
University of Utah Interdisciplinary Training Program in Computational Approaches to Diabetes and Metabolism ResearchT32DK110966 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Karen Louise Eilbeck, Marcus Guy Pezzolesi · 2016 to 2026
$2.6M
NHLBI NIH HHS R01 HL149870NIDDK NIH HHS T32 DK110966
6 · The paper itself

Abstract

This review provides a holistic perspective on the bi-directional relationship between cardiac mitochondrial dysfunction and myocardial structural remodeling in the context of metabolic heart disease, natural cardiac aging, and heart failure. First, a review of the physiologic and molecular drivers of cardiac mitochondrial dysfunction across a range of increasingly prevalent conditions such as metabolic syndrome and cardiac aging is presented, followed by a general review of the mechanisms of mitochondrial quality control (QC) in the heart. Several important mechanisms by which cardiac mitochondrial dysfunction triggers or contributes to structural remodeling of the heart are discussed: accumulated metabolic byproducts, oxidative damage, impaired mitochondrial QC, and mitochondrial-mediated cell death identified as substantial mechanistic contributors to cardiac structural remodeling such as hypertrophy and myocardial fibrosis. Subsequently, the less studied but nevertheless important reverse relationship is explored: the mechanisms by which cardiac structural remodeling feeds back to further alter mitochondrial bioenergetic function. We then provide a condensed pathogenesis of several increasingly important clinical conditions in which these relationships are central: diabetic cardiomyopathy, age-associated declines in cardiac function, and the progression to heart failure, with or without preserved ejection fraction. Finally, we identify promising therapeutic opportunities targeting mitochondrial function in these conditions.

Indexed as

cardiacfibroblastsfibrosisMitochondriamitophagyremodeling

Identifiers

PMID36742465
PMCPMC9894375
OpenAlexW4313522434

What OpenQuestion 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 OpenQuestion graph.