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Mitochondrial Fission and Fusion Factors Reciprocally Orchestrate Mitophagic Culling in Mouse Hearts and Cultured Fibroblasts
Open accessAbstract
How mitochondrial dynamism (fission and fusion) affects mitochondrial quality control is unclear. We uncovered distinct effects on mitophagy of inhibiting Drp1-mediated mitochondrial fission versus mitofusin-mediated mitochondrial fusion. Conditional cardiomyocyte-specific Drp1 ablation evoked mitochondrial enlargement, lethal dilated cardiomyopathy, and cardiomyocyte necrosis. Conditionally ablating cardiomyocyte mitofusins (Mfn) caused mitochondrial fragmentation with eccentric remodeling and no cardiomyocyte dropout. Parallel studies in cultured murine embryonic fibroblasts (MEFs) and in vivo mouse hearts revealed that Mfn1/Mfn2 deletion provoked accumulation of defective mitochondria exhibiting an unfolded protein response, without appropriately increasing mitophagy. Conversely, interrupting mitochondrial fission by Drp1 ablation increased mitophagy and caused a generalized loss of mitochondria. Mitochondrial permeability transition pore (MPTP) opening in Drp1 null mitochondria was associated with mitophagy in MEFs and contributed to cardiomyocyte necrosis and dilated cardiomyopathy in mice. Drp1, MPTP, and cardiomyocyte mitophagy are functionally integrated. Mitochondrial fission and fusion have opposing roles during in vivo cardiac mitochondrial quality control.
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“Moreover, Mfn2 has been shown to participate in mitophagy in cardiomyocytes (Chen & Dorn, 2013; Song et al, 2015).”
From Mfn2 deficiency links age‐related sarcopenia and impaired autophagy to activation of an adaptive mitophagy pathway (2016) · cites this paper as Song et al, 2015
In the citing paper
“Impairment of fission leads to the disruption of selective mitochondrial autophagic degradation, followed by dysfunctional organelles accumulation [58, 196–200].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [200]
In the citing paper
“Disrupted mitochondrial fission, obtained with the specific ablation of DRP1 in the heart, induces accumulation of defective mitochondria due to impaired autophagy/mitophagy, that over-time promotes cardiomyocyte death [198–200].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [200]
In the citing paper
“Consistent with this crucial role, conditional ablation of DRP1 in the heart, brain, and skeletal muscle causes lethality [196, 198–200, 208, 209].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [200]
In the citing paper
“Energy stress consequent to acute or chronic exercise triggers autophagy in different tissues [197–200].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [200]
In the citing paper
“Mitophagy is intricately linked to mitochondrial dynamics [180,181,182].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [181]
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“This is highlighted by several observations: Increased fission fails to initiate death (Chen et al., 2005; Papanicolaou et al., 2012; Song et al., 2015; Song and Dorn, 2015) and improves stress-resistance (Papanicolaou et al.”
BackgroundResultInfluentialPeroxiredoxin 6 Modulates Insulin Secretion and Beta Cell Death via a Mitochondrial Dynamic Network
Pacifici, F., Della‐Morte, D., Capuani, B., Coppola, A., Scioli, M. G., Donadel, G., Andreadi, A., Ciccosanti, F., Fimia, G. M., Bellia, A., et al. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.842575 · Cited by 10
“Among these, a lack of mitofusin blunts both mitophagy and autophagy, leading to an accumulation of small fragmented and damaged mitochondria (38, 39).”
BackgroundA lack of ChREBP inhibits mitochondrial cristae formation in brown adipose tissue
Sakiyama, H., Li, L., Kuwahara‐Otani, S., Nakagawa, T., Eguchi, H., Yoshihara, D., Shinohara, M., Fujiwara, N., & Suzuki, K. (2021) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-021-04178-2 · Cited by 11
Role of Autophagy in Myocardial Remodeling After Myocardial Infarction
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RetractedEnergy metabolism and redox balance: How phytochemicals influence heart failure treatment
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EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis
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Mitochondria in pathological cardiac remodeling
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Cardiac energy metabolism in heart failure
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“Mitochondria containing damaged mtDNA, abnormal proteins, or oxidized lipids are efficiently removed by mitophagy to maintain homeostasis of the organelle [43].”
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Post-Translational Modification of Drp1 is a Promising Target for Treating Cardiovascular Diseases
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“Drp1 is a key protein in mitochondrial biological processes, and heart failure models in cardiac-specific Drp1 knockout mice have demonstrated the important role of Drp1 in maintaining normal cardiac function [114].”
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“active role in mitochondrial fission, suggested to be a prerequisite step for mitochondrial autophagy.(12,14) Whether Drp1-dependent fission is mechanistically linked to Drp1-”
BackgroundDrp1 knockdown aggravates obesity-induced cardiac dysfunction and remodeling
Wu, D., Hu, Q., Li, H., Yin, Y., Wang, P., & Wang, W. (2025) · Mitochondrion · doi:10.1016/j.mito.2025.102023 · Cited by 6
Monitoring Mitochondrial Morphology and Respiration in Doxorubicin-Induced Cardiomyopathy
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Correcting abnormal mitochondrial dynamics to facilitate tumor treatment
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Neurohormonal connections with mitochondria in cardiomyopathy and other diseases
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Mitochondrial dynamics regulate cell morphology in the developing cochlea
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BackgroundDrp1 regulates transcription of ribosomal protein genes in embryonic hearts
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Metadata
- Authors
- Song, M., Mihara, K., Chen, Y., Scorrano, L., & Dorn, G. W.
- Affiliations
- Washington University in St. Louis (US)
- Kyushu University (JP)
- University of Padua (IT)
- Corresponding author
- Dorn, Gerald W.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 21
- Issue
- 2
- Pages
- 273-286
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC4318753
- OpenAlex
- W2044929466
- Cited by
- 482
- References
- 47
- Citations by year
- 2026: 21 · 2025: 31 · 2024: 51 · 2023: 42 · 2022: 42 · 2021: 63 · 2020: 55 · 2019: 43 · 2018: 39 · 2017: 33 · 2016: 40 · 2015: 21
- FWCI
- 19.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- Japan Society for the Promotion of Science (25291046)
- National Heart, Lung, and Blood Institute (HL59888, R01HL059888)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- mitochondrial fission, mitochondrial fusion, mitophagy, Drp1, mitofusins, Mfn1, mitofusin 2, mitochondrial quality control, myocardial necrosis, dilated cardiomyopathy, mitochondrial permeability transition pore, unfolded protein response, mitochondrial fragmentation, embryonic fibroblasts, heart
- MeSH terms
- Animals, Cells, Cultured, Fibroblasts, Mice, Transgenic, Mitochondria, Heart, Myocardium, Mice, Knockout, GTP Phosphohydrolases, Dynamins, Mice, Mitochondrial Dynamics, Mitophagy
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