Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice
Abstract
A change of heart (mitochondria): Mitochondria provide an essential source of energy to drive cellular processes and are particularly important in heart muscle cells (see the Perspective by Gottlieb and Bernstein). After birth, the availability of oxygen and nutrients to organs and tissues changes. This invokes changes in metabolism. Gong et al. studied the developmental transitions in mouse heart mitochondria soon after birth. Mitochondria were replaced wholesale via mitophagy in cardiomyocytes over the first 3 weeks after birth. Preventing this turnover by interfering with parkin-mediated mitophagy specifically in cardiomyocytes prevented the normal metabolic transition and caused heart failure. Thus, the heart has coopted a quality-control pathway to facilitate a major developmental transition after birth. Wai et al. examined the role of mitochondrial fission and fusion in mouse cardiomyocytes. Disruption of these processes led to “middle-aged” death from a form of dilated cardiomyopathy. Mice destined to develop cardiomyopathy were protected by feeding with a high-fat diet, which altered cardiac metabolism. Science , this issue p. 10.1126/science.aad2459 , p. 10.1126/science.aad0116 ; see also p. 1162
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Germline deletion of OMA1 does not impair embryogenesis, indicating that OMA1-induced OPA1 processing is dispensable for embryonic and adult mouse development.
“In contrast to Yme1L1, the germline deletion of OMA1 does not impair embryogenesis, which indicates that OMA1-induced OPA1 processing is dispensable for embryonic and adult mouse development [166, 167].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [166]
In mice, total genetic ablation of Yme1L1 leads to embryonic death.
“In mice, total genetic ablation of Yme1L1 leads to embryonic death, while the specific inhibition of the gene in the heart causes dilated cardiomyopathy that shortens lifespan (median life span:46 weeks).”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [166]
Cardiac function and lifespan of mice lacking YME1L in cardiomyocytes are normalized without restoring mitochondrial morphology when deletion of YME1L happens in both cardiomyocytes and skeletal muscle fibers, with median life span 125 weeks.
“Interestingly, cardiac function and lifespan of mice lacking YME1L in cardiomyocytes are normalized without restoring mitochondrial morphology, when the deletion of YME1L happens in both cardiomyocytes and skeletal muscle fibers (median life span 125 weeks).”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [166]
Double deletion of Yme1L1 and OMA1 specifically in the heart restored mitochondrial morphology and rescued cardiac function.
“In agreement, double deletion of Yme1L1 and OMA1, specifically in the heart, restored mitochondrial morphology and rescued cardiac function [166].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [166]
The recovery of cardiac function and lifespan in mice lacking YME1L in both cardiomyocytes and skeletal muscle is because loss of YME1L in skeletal muscle and consequent mitochondrial dysfunction triggers systemic glucose intolerance and lowers insulin levels, preventing cardiac glucose overload and cardiomyopathy.
“This recovery is because the loss of YME1L in skeletal muscle and the consequent mitochondrial dysfunction triggers systemic glucose intolerance and lowers insulin levels preventing cardiac glucose overload and cardiomyopathy [166].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [166]
Specific inhibition of Yme1L1 in the heart causes dilated cardiomyopathy that shortens lifespan, with median life span 46 weeks.
“In mice, total genetic ablation of Yme1L1 leads to embryonic death, while the specific inhibition of the gene in the heart causes dilated cardiomyopathy that shortens lifespan (median life span:46 weeks).”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [166]
YME1L ablation in cardiomyocytes activates OMA1 and promotes OPA1 processing and mitochondrial fragmentation, causing heart failure.
“Mechanistically, YME1L ablation in cardiomyocytes activates OMA1 and promotes OPA1 processing and mitochondrial fragmentation, which causes heart failure [166].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [166]
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- Authors
- Wai, T., García-Prieto, J., Baker, M. J., Merkwirth, C., Benit, P., Rustin, P., Rupérez, F. J., Barbas, C., Ibañez, B., & Langer, T.
- Affiliations
- University of Cologne (DE)
- Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
- INSERM UMR 1141, Hôpital Robert Debré, Paris, France.
- Inserm (FR)
- Universidad San Pablo CEU (ES)
- Corresponding author
- Wai, Timothy
- Langer, Thomas
- Venue
- Science
- Published
- 2015-12-04
- Volume
- 350
- Issue
- 6265
- Pages
- aad0116-aad0116
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2190642228
- Cited by
- 551
- References
- 72
- Citations by year
- 2026: 40 · 2025: 47 · 2024: 55 · 2023: 66 · 2022: 68 · 2021: 64 · 2020: 48 · 2019: 41 · 2018: 49 · 2017: 50 · 2016: 22 · 2015: 1
- FWCI
- 17.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- HAL (submittedVersion)
- Funders
- European Research Council
- Deutsche Forschungsgemeinschaft
- Spanish Ministry of Economy and Competitiveness (MINECO)
- Human Frontiers Science Program
- ERDF/FEDER
- Networks for Cooperative Research in Health (RETIC) (RD12/0042/0054)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- OPA1, mitochondrial fission, mitochondrial fusion, mitochondrial fragmentation, heart failure, cardiomyocytes, mitophagy, Parkin, postnatal heart development, myocardial metabolism, dilated cardiomyopathy, high-fat diet, mitochondrial quality control
- MeSH terms
- Animals, Cardiomyopathy, Dilated, Female, Heart, Heart Failure, Male, Metalloendopeptidases, Mitochondria, Heart, Myocardium, Gene Deletion, Mice, Knockout, Muscle, Skeletal, GTP Phosphohydrolases, Mitochondrial Proteins, Myocytes, Cardiac, Metalloproteases, Embryonic Development, Mice, Diet, High-Fat, Proteolysis, Mitochondrial Dynamics, Mitophagy
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