Evidence map›Paper›PMID 39026280›Full record

ReviewCardiovascular diabetology2024

Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction.

Michael W Rudokas, Margaret McKay, Zeren Toksoy, Julia N Eisen, Markus Bögner, Lawrence H Young, Fadi G Akar

Abstract readReview
In one paragraph

Review in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 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.

Michael W RudokasDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, USA.
Margaret McKayDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, USA.
Zeren ToksoyDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, USA.
Julia N EisenDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, USA.
Markus BögnerDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, USA.
Lawrence H YoungDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, USA.
Fadi G AkarDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, New Haven, CT, USA. fadi.akar@yale.edu.

Funding

Metabolic signaling in atrial fibrillation and remodelingR01HL148008 · NHLBI · YALE UNIVERSITY · PI AKAR, FADI GABRIEL, YOUNG, LAWRENCE H · 2021 to 2024
$2.2M
Mitochondrial fission in diabetes-related arrhythmiaR01HL149344 · NHLBI · YALE UNIVERSITY · PI AKAR, FADI GABRIEL · 2020 to 2023
$1.7M
Optimizing AF ablation by a novel optogenetics and computational approachR21HL165147 · NHLBI · YALE UNIVERSITY · PI AKAR, FADI GABRIEL · 2022 to 2023
$461k
Regulating Mitochondrial Fission for Arrhythmia PreventionR21HL114378 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI AKAR, FADI GABRIEL · 2013 to 2014
$448k
NHLBI NIH HHS R01 HL148008NHLBI NIH HHS R01 HL149344NHLBI NIH HHS R21 HL114378NHLBI NIH HHS R21 HL165147NIH HHS R01 HL148008NIH HHS R01 HL149344
6 · The paper itself

Abstract

Mitochondria play a central role in cellular energy metabolism, and their dysfunction is increasingly recognized as a critical factor in the pathogenesis of diabetes-related cardiac pathophysiology, including vulnerability to ischemic events that culminate in myocardial infarction on the one hand and ventricular arrhythmias on the other. In diabetes, hyperglycemia and altered metabolic substrates lead to excessive production of reactive oxygen species (ROS) by mitochondria, initiating a cascade of oxidative stress that damages mitochondrial DNA, proteins, and lipids. This mitochondrial injury compromises the efficiency of oxidative phosphorylation, leading to impaired ATP production. The resulting energy deficit and oxidative damage contribute to functional abnormalities in cardiac cells, placing the heart at an increased risk of electromechanical dysfunction and irreversible cell death in response to ischemic insults. While cardiac mitochondria are often considered to be relatively autonomous entities in their capacity to produce energy and ROS, their highly dynamic nature within an elaborate network of closely-coupled organelles that occupies 30-40% of the cardiomyocyte volume is fundamental to their ability to exert intricate regulation over global cardiac function. In this article, we review evidence linking the dynamic properties of the mitochondrial network to overall cardiac function and its response to injury. We then highlight select studies linking mitochondrial ultrastructural alterations driven by changes in mitochondrial fission, fusion and mitophagy in promoting cardiac ischemic injury to the diabetic heart.

Indexed as

Diabetic CardiomyopathiesEnergy MetabolismMitochondria, HeartMyocardial IschemiaOxidative StressAnimalsHumansMitochondrial DynamicsMitophagyMyocytes, CardiacReactive Oxygen SpeciesSignal TransductionReactive Oxygen SpeciesArrhythmiaDiabetesIschemiaIschemia-reperfusion injuryMitochondriaMitochondrial dynamicsROS-induced ROS-releaseROS (reactive oxygen species)

Identifiers

PMID39026280
PMCPMC11264840

What Socratic holds

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LicenceCC BY
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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 Socratic graph.