ArticleCirculation research2012
Mitofusins 1 and 2 are essential for postnatal metabolic remodeling in heart.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 1 of them a synthesis that pooled it.
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Who cites it
148 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.
- Reprogramming heart failure: physiological orchestration and mechanistic decoding of exercise benefits.BMC cardiovascular disorders · 2025Pooled it
- Mitofusin 2 polymorphic variants and left ventricular hypertrophy in human hypertension.Journal of human hypertension · 2026Article
- Loss of the mitochondrial SAM transporter reveals a lipoylation-dependent metabolic vulnerability in the postnatal heart.Science advances · 2026Article
- Inhibition of RBM25 preserves cardiac mitochondrial homeostasis and attenuates ischemic heart failure.Journal of molecular histology · 2026Article
- Smarca4 maintains mitochondrial homeostasis and energy metabolism during cardiac development.Cellular and molecular life sciences : CMLS · 2026Article
- Cys340Ser Mutation Abolishing S-Nitrosylation Drives GRK2 Mitochondrial Localization and Dysfunction.Cells · 2026Article
- Metabolic-epigenetic axis in cardiovascular inflammatory injury: regulatory mechanisms and intervention strategies.Frontiers in cardiovascular medicine · 2026Review
- Nonstructural Roles of Junctophilin-2 in the Heart.JACC. Basic to translational science · 2025Review
- Mitochondrial quality control in cardiomyocytes: safeguarding the heart against disease and ageing.Nature reviews. Cardiology · 2025Review
- Article
- Selected Pathway Analyses to Gain Mechanistic Insights into the Pathogenesis of Feline Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2025Article
- Mitochondrial metabolic maturation in postnatal right ventricle restricted by volume overload.Intractable & rare diseases research · 2025Article
- Mitochondrial DNA depletion syndrome and its cardiac complication.Frontiers in cardiovascular medicine · 2025Review
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- Klf9 is essential for cardiac mitochondrial homeostasis.Nature cardiovascular research · 2024Article
- SIRT6 in Regulation of Mitochondrial Damage and Associated Cardiac Dysfunctions: A Possible Therapeutic Target for CVDs.Cardiovascular toxicology · 2024Review
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Hemodynamic Melody of Postnatal Cardiac and Pulmonary Development in Children with Congenital Heart Diseases.Biology · 2024Review
- Cellular Senescence, Mitochondrial Dysfunction, and Their Link to Cardiovascular Disease.Cells · 2024Review
- Mitochondrial non-energetic function and embryonic cardiac development.Frontiers in cell and developmental biology · 2024Review
88 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
rationaleAt birth, there is a switch from placental to pulmonary circulation and the heart commences its aerobic metabolism. In cardiac myocytes, this transition is marked by increased mitochondrial biogenesis and remodeling of the intracellular architecture. The mechanisms governing the formation of new mitochondria and their expansion within myocytes remain largely unknown. Mitofusins (Mfn-1 and Mfn-2) are known regulators of mitochondrial networks, but their role during perinatal maturation of the heart has yet to be examined.
objectiveThe objective of this study was to determine the significance of mitofusins during early postnatal cardiac development. METHODS AND
resultsWe genetically inactivated Mfn-1 and Mfn-2 in midgestational and postnatal cardiac myocytes using a loxP/Myh6-cre approach. At birth, cardiac morphology and function of double-knockout (DKO) mice are normal. At that time, DKO mitochondria increase in numbers, appear to be spherical and heterogeneous in size, but exhibit normal electron density. By postnatal day 7, the mitochondrial numbers in DKO myocytes remain abnormally expanded and many lose matrix components and membrane organization. At this time point, DKO mice have developed cardiomyopathy. This leads to a rapid decline in survival and all DKO mice die before 16 days of age. Gene expression analysis of DKO hearts shows that mitochondria biogenesis genes are downregulated, the mitochondrial DNA is reduced, and mitochondrially encoded transcripts and proteins are also reduced. Furthermore, mitochondrial turnover pathways are dysregulated.
conclusionsOur findings establish that Mfn-1 and Mfn-2 are essential in mediating mitochondrial remodeling during postnatal cardiac development, a time of dramatic transitions in the bioenergetics and growth of the heart.
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Registered trials
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