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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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Citations
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Self-citationMitochondrial dynamics and their potential as a therapeutic target
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“…in mammalian cells (Tanaka et al., 2010; Rambold et al., 2011; Kageyama et al., 2014; Ikeda et al., 2015), a limited number of studies have also reported that Dnm1/Drp1 are not required for mitophagy in yeast (Mendl et al., 2011; Bernhardt et al., 2015) and in mammalian cells (Song et al., 2015).”
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“Results Parkin Is Upregulated in Mitochondrial Fission– Defective Mouse Hearts Interrupting mitochondrial fission by cardiac myocyte–specific Drp1 ablation induces cardiomyopathy with loss of mitochondria (Online Figure I).8 Parkin localization to, and mitophagy of, mitochondria in Drp1-deficient cultured mouse embryo…”
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Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction
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“administration of tamoxifen (20 mg/kg/day) (Myh6-MerCreMer inducible model).(39) WT control mice were flx/flx littermates injected with tamoxifen, but lacking the Cre-recombinase gene.”
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Evolving Concepts of Mitochondrial Dynamics
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“Deletion of MFN1 and MFN2 suppressed mitophagy in mouse embryonic fibroblasts and cardiomyocytes (20, 21).”
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Pagliuso, A., Cossart, P., & Stavru, F. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2603-0 · Cited by 192
Mitofusins regulate lipid metabolism to mediate the development of lung fibrosis
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Self-citationSarcoplasmic reticulum–mitochondria communication in cardiovascular pathophysiology
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Mitochondrial quality control: from molecule to organelle
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“Alterations in mitochondrial quality control responses have been described in several mitochondrial diseases such as neurodegenerative diseases (Parkinson’s, Alzheimer’s and Huntington’s disease) [8–11], cardiomyopathies [12], ocular diseases [13, 14] and cancer [15–17], highlighting the importance of an adequate bala…”
BackgroundTitration of mitochondrial fusion rescues Mff -deficient cardiomyopathy
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Mitohormesis, an Antiaging Paradigm
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“Thus, fission/fusion, mitophagy, and biogenesis converge to constitute the process of mitochondrial quality control (15, 40).”
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“Although early studies, using Fis1 overexpression and inhibition, support pivotal roles of Fis1 during mitochondrial fission, a follow-up investigation in cancer cell lines shows that Fis1 deletion does not impair Drp1 recruitment and mitochondrial morphology (reviewed in detail by Chan, 2012).”
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“Indeed, since interfering with mitochondrial fusion produces mitochondrial shortening both in vitro and in vivo (Chen et al, 2003, 2011; Song et al, 2015), mitochondrial enlargement in multiple models of organ-specific in vivo Mfn2 insufficiency seems to rule out defective fusion as the principal…”
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“Furthermore, loss of mitochondrial biogenesis through an imbalance of mitophagy and mitochondrial fission/fusion and accumulation of mitochondrial debris leads to cardiac ageing in mice [39, 40].”
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Novel targets for mitochondrial medicine
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“(179) Drp1 CM-specific (Myh6 nucleardirected Cre) KO after birth Neonatal cardiomyopathy (94); modestly enlarged hearts (179) Connected or enlarged mitochondria (94) Mitochondrial respiration 2 (94); Parkin-independent mitophagy signaling 1 (94) Died at 1–1.”
BackgroundPhysical Exercise: A Novel Tool to Protect Mitochondrial Health
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Targeting mitochondrial fusion and fission proteins for cardioprotection
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“A large number of studies have shown that normal mitochondrial function depends on normal mitochondrial dynamics (Song et al., 2015).”
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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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