Glancy B, Hartnell LM, Combs CA, Femnou A, Sun J, Murphy E, Subramaniam S, Balaban RS.Glancy B, et al.Cell Rep. 2018 May 29;23(9):2832. doi: 10.1016/j.celrep.2018.05.055.Cell Rep. 2018.PMID: 29847811Free PMC article.No abstract available.
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.
3D electron microscopy; energy distribution; mitochondrial dynamics; mitochondrial retraction; muscle energetics; oxidative phosphorylation.
Kim S, Song J, Ernst P, Latimer MN, Ha CM, Goh KY, Ma W, Rajasekaran NS, Zhang J, Liu X, Prabhu SD, Qin G, Wende AR, Young ME, Zhou L.Kim S, et al.Am J Physiol Heart Circ Physiol. 2020 Mar 1;318(3):H682-H695. doi: 10.1152/ajpheart.00617.2019. Epub 2020 Jan 31.Am J Physiol Heart Circ Physiol. 2020.PMID: 32004065
Khadangi A, Hanssen E, Rajagopal V.Khadangi A, et al.BMC Med Inform Decis Mak. 2019 Dec 19;19(Suppl 6):272. doi: 10.1186/s12911-019-0962-1.BMC Med Inform Decis Mak. 2019.PMID: 31856827Free PMC article.