Power Grid Protection of the Muscle Mitochondrial Reticulum
Open accessAbstract
Mitochondrial network connectivity enables rapid communication and distribution of potential energy throughout the cell. However, this connectivity puts the energy conversion system at risk, because damaged elements could jeopardize the entire network. Here, we demonstrate the mechanisms for mitochondrial network protection in heart and skeletal muscle (SKM). We find that the cardiac mitochondrial reticulum is segmented into subnetworks comprising many mitochondria linked through abundant contact sites at highly specific intermitochondrial junctions (IMJs). In both cardiac and SKM subnetworks, a rapid electrical and physical separation of malfunctioning mitochondria occurs, consistent with detachment of IMJs and retraction of elongated mitochondria into condensed structures. Regional mitochondrial subnetworks limit the cellular impact of local dysfunction while the dynamic disconnection of damaged mitochondria allows the remaining mitochondria to resume normal function within seconds. Thus, mitochondrial network security is comprised of both proactive and reactive mechanisms in striated muscle cells.
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IMJs are detached in dysfunctional mitochondria, promoting electrical isolation and further segregation of the malfunctioning organelle from the network.
“To prevent the spread of dysfunction, IMJs are detached in dysfunctional mitochondria, promoting the electrical isolation and further segregation from the network of the malfunctioning organelle [28].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [28]
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- Authors
- Glancy, B., Hartnell, L. M., Combs, C. A., Femnou, A., Sun, J., Murphy, E., Subramaniam, S., & Balaban, R. S.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Glancy, Brian
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2017-04
- Volume
- 19
- Issue
- 3
- Pages
- 487-496
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC5490369
- OpenAlex
- W2606122737
- Cited by
- 172
- References
- 32
- Citations by year
- 2026: 6 · 2025: 14 · 2024: 10 · 2023: 19 · 2022: 21 · 2021: 31 · 2020: 24 · 2019: 27 · 2018: 18 · 2017: 2
- FWCI
- 7.93
- Type
- journal article
- Language
- en
- Update notices
- erratum (2018-05-29)
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- DIR NHLBI (1ZIAHL004610-09)
- CCR, NCI (1ZIABC010278-19)
- 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
- mitochondrial reticulum, mitochondrial contact sites, mitochondrial dysfunction, myocardium, skeletal muscle, mitochondrial segregation, striated muscle cells, energy conversion
- MeSH terms
- Animals, Energy Metabolism, Male, Mice, Inbred C57BL, Mitochondria, Heart, Mitochondria, Muscle, Membrane Potential, Mitochondrial
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