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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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Myoglobin induces mitochondrial fusion, thereby inhibiting breast cancer cell proliferation
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“Fission and fusion are involved in the elimination of damaged/dysfunctional mitochondria (Song et al., 2015) which may serve as major sources of ROS.”
BackgroundDynamin-related protein 1 mediates low glucose-induced endothelial dysfunction in human arterioles
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BackgroundResveratrol reduces the apoptosis induced by cigarette smoke extract by upregulating MFN2
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Self-citationMtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis
Patitucci, C., Hernández‐Camacho, J. D., Vimont, E., Yde, S., Cokelaer, T., Chaze, T., Gianetto, Q. G., Matondo, M., Gazi, A. D., Nemazanyy, I., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-44143-9 · Cited by 32
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“Mitochondrial Permeability Transition Pore Opening Mitochondrial permeability transition pore (mPTP) opening induced by calcium was determined in freshly isolated cardiac mitochondria (13).”
BackgroundMethodMitophagy in cardiovascular homeostasis
Zhang, R., Krigman, J., Luo, H., Ozgen, S., Yang, M., & Sun, N. (2020) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2020.111245 · Cited by 31
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“Drp1 deficiency in adult mouse hearts showed the pathophysiological consequences of progressive ventricular enlargement and functional decompensation, resulting in heart failure (80).”
BackgroundCentral Parkin: The evolving role of Parkin in the heart
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“Moreover, genetic ablation of the fusion protein mitofusin 1/2 (Mfn1/2) or the fission protein dynamin related protein 1 (Drp1) was found to provoke only modest changes in mitochondrial size in contrast to significant energetics and functional outcomes in adult ventricular myocytes (Ikeda et al. 2015; Song et al. 2015…”
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“The Role DRP1 Acts in a Cachexia Model in vitro Lately, it was reported that the DRP1 level was crucial for mitochondrial function and muscle physiology (Romanello et al., 2010; Song et al., 2015; Favaro et al., 2019; Romanello and Sandri, 2021).”
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Li, A. S., Shami, G. J., Griffiths, L. M., Lal, S., Irving, H. R., & Braet, F. (2023) · Basic Research in Cardiology · doi:10.1007/s00395-023-01011-3 · Cited by 29
“If the damaged mitochondria fail to be recycled by autophagosomes they can fuse with healthy mitochondria [63], and thus contributing to the formation of giant mitochondria.”
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“Neuron-specific deletion of Drp1 leads to mitochondrial dysfunction and neurodegeneration in the brain, while cardiomyocyte-specific deletion of Drp1 causes heart failure.(14-18) At the cellular level, the loss of Drp1 enlarges mitochondria due to unopposed mito-”
BackgroundCardiac mitofusin-1 is reduced in non-responding patients with idiopathic dilated cardiomyopathy
Hsiao, Y., Shimizu, I., Wakasugi, T., Yoshida, Y., Ikegami, R., Hayashi, Y., Suda, M., Katsuumi, G., Nakao, M., Ozawa, T., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-86209-y · Cited by 26
Mitochondria regulate cardiac contraction through ATP-dependent and independent mechanisms
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“This indicates that moderate shifts in fission/ fusion are not inherently detrimental to the heart, unlike the more robust disruption induced by specific deletion of fission and fusion genes [35, 36, 38, 45].”
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Mitochondrial Dysfunction in Arrhythmia and Cardiac Hypertrophy
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“Similarly, cardiomyocyte-specific knockout of Drp1 mice died at 6 weeks of age [116].”
BackgroundNew Insights Into the Role of Mitochondria Quality Control in Ischemic Heart Disease
Xin, Y., Zhang, X., Li, J., Gao, H., Li, J., Li, J., Hu, W., & Li, H. (2021) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2021.774619 · Cited by 28
“(90) found that conditional ablation of Drp1 in mouse embryonic fibroblasts promoted mPTP-mediated mitophagy.”
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Mani, K. M., Javaheri, A., & Diwan, A. (2018) · Comprehensive physiology · doi:10.1002/cphy.c180005 · Cited by 29
Disruption of cTnT-Mediated Sarcomere–Mitochondrial Communication Results in Dilated Cardiomyopathy
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All-Trans Retinoic Acid Increases DRP1 Levels and Promotes Mitochondrial Fission
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FAK regulates cardiomyocyte mitochondrial fission and function through Drp1
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Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment
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“CM necrosis is characterized by the rupture of the plasma membrane and estimated using the Evans blue dye uptake assay as described previously [25].”
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“96 Mitochondrial fragmentation and dysfunction have been observed in human myocardium from patients with pressure overload or IHD with preserved or reduced ejection fraction.”
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“[88] Additionally, MFN1/Mfn2 double knockout leads to the accumulation of defective mitochondria, hinting at an unexplored role of Mfn2 in MQC. [89,90] Unlike MFN1/2, the role of Opa1 in cardioprotection is well documented.”
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NovelDNM1Lvariants impair mitochondrial dynamics through divergent mechanisms
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“Furthermore, cardiac-speci fi c (Ashra fi an et al, 2010; Ikeda et al, 2015; Ishihara et al, 2015; Song et al, 2015) and brain-speci fi c (Ishihara et al, 2009; Wakabayashi et al, 2009) ablation of DRP1 leads to lethal dilated cardiomyopathy and defective cerebellar development with early postnatal…”
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“Thus, Drp1 knock-out mice display embryonic lethality, increased mitophagy and dilated cardiomyopathy, associated with increased levels of necrotic cell death, as well as abnormal brain development and failure to develop synapses (Ishihara et al., 2009; Wakabayashi et al., 2009; Song et al., 2015).”
BackgroundA Mitochondrial Approach to Cardiovascular Risk and Disease
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“5), smaller, and rounder than the mitochondria of fibroblasts [6].”
BackgroundRetractedNek4 regulates mitochondrial respiration and morphology
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“This can occur through asymmetric fission with the segregation of functional from dysfunctional mitochondrial components into different daughter mitochondria, and the subsequent elimination of the resultant dysfunctional mitochondria through mitophagy [6].”
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“5) and in other tissues (Bhandari et al., 2015; Chen et al., 2003; Song et al., 2015).”
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“Drp1, a key component of the mitochondrial fission system, plays a crucial role in regulating the homeostasis between fission and fusion, and in maintaining mitochondrial morphology (Song et al., 2015).”
BackgroundMitochondrial fission is a critical modulator of mutant APP-induced neural toxicity
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Mitochondrial Genome Variants as a Cause of Mitochondrial Cardiomyopathy
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Mitochondrial Dysfunction in the Cardio-Renal Axis
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“On the other hand, cardiac Mfn2 ablation interrupts the autophagic removal of mitochondria from cardiomyocytes and leads to the accumulation of mitochondria without increasing mitophagy ( 63 , 67 ).”
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“Animal Care and Use Committee, under the title “the role of LYCAT in lung cancer” (16-203).”
Background
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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