Research progress on the role of canonical transient receptor potential channels in skeletal muscle diseases

doi:10.16352/j.issn.1001-6325.2023.08.1309

Abstract

Abstract: Canonical transient receptor potential(TRPC) is a kind of non-selective cation channel located in the cell membrane, which plays an important role in electrophysiological activity of cells. Under pathological conditions, TRPC channels are more selective for Ca²⁺, which will break the Ca²⁺ homeostasis in skeletal muscle cells and lead to calcium overload and subsequent occurrence of a variety of skeletal muscle diseases. To study the role and mechanism of TRPC channels in skeletal muscle diseases is helpful to provide new ideas for disease treatment.

Key words: canonical transient receptor potential(TRPC) channel, skeletal muscle, skeletal muscle diseases, calcium ions

CLC Number:

XIE Dongge, LI Junhao, HAN Han, LI Shoutian. Research progress on the role of canonical transient receptor potential channels in skeletal muscle diseases[J]. Basic & Clinical Medicine, 2023, 43(8): 1309-1312.

References 24

[1]	Jeon J, Bu F, Sun G, et al. Contribution of TRPC channels in neuronal excitotoxicity associated with neurodegenerative disease and ischemic stroke[J]. Front Cell Dev Biol, 2021,8:618663.doi:10.3389/fcell.2020.618663.
[2]	Sierra-Valdez F, Azumaya CM, Romero LO, et al. Structure-function analyses of the ion channel TRPC3 reveal that its cytoplasmic domain allosterically modulates channel gating[J].J Biol Chem,2018,293:16102-16114.
[3]	Erkan-Candag H, Clarke A, Tiapko O, et al. Diacylglycerols interact with the L2 lipidation site in TRPC3 to induce a sensitized channel state[J]. EMBO Rep, 2022,e54276.doi:10.15252/embr.202154276.
[4]	Numaga-Tomita T, Oda S, Nishiyama K, et al. TRPC channels in exercise-mimetic therapy[J]. Pflugers Arch, 2019,471:507-517.
[5]	Li Z, Zhou J, Li Y, et al. Mitochondrial TRPC3 promotes cell proliferation by regulating the mitochondrial calcium and metabolism in renal polycystin-2 knockdown cells[J]. Int Urol Nephrol,2019,51:1059-1070.doi:10.1007/s11255-019-02149-7.
[6]	Guo W, Tang Q, Wei M, et al. Structural mechanism of human TRPC3 and TRPC6 channel regulation by their intracellular calcium-binding sites[J]. Neuron, 2022,110:1023-1035.
[7]	Hogarth MW, Houweling PJ, Thomas KC, et al. Evidence for ACTN3 as a genetic modifier of Duchenne muscular dystrophy[J].Nat Commun, 2017,8:14143.doi:10.1038/ncomms14143.
[8]	Woo JS, Cho CH, Kim DH, et al. TRPC3 cation channel plays an important role in proliferation and differentiation of skeletal muscle myoblasts[J]. Exp Mol Med, 2010,42:614-627.
[9]	Chung HS, Kim GE, Holewinski RJ, et al. Transient receptor potential channel 6 regulates abnormal cardiac S-nitrosylation in Duchenne muscular dystrophy[J]. Proc Natl Acad Sci U S A, 2017,114:E10763-E10771.
[10]	Schiavone M, Zulian A, Menazza S, et al. Alisporivir rescues defective mitochondrial respiration in Duchenne muscular dystrophy[J]. Pharmacol Res, 2017,125:122-131.
[11]	Rocha GLD, Rupcic IF, Mizobuti DS, et al. Cross-talk between TRPC-1, mTOR, PGC-1α and PPARδ in the dystrophic muscle cells treated with tempol[J]. Free Radic Res, 2022,56:245-257.
[12]	Lopez JR, Uryash A, Faury G, et al. Contribution of TRPC channels to intracellular Ca2+ dyshomeostasis in smooth muscle from mdx mice[J]. Front Physiol, 2020,11:126.doi:10.3389/fphys.2020.00126.
[13]	Creisméas A, Gazaille C, Bourdon A, et al. TRPC3, but not TRPC1, as a good therapeutic target for standalone or complementary treatment of DMD[J]. Transl Med, 2021,19:519. Published 2021 Dec 20.doi:10.1186/s12967-021-03191-9.
[14]	Pradhan BS, Prószyński TJ. A role for caveolin-3 in the pathogenesis of muscular dystrophies[J]. Int J Mol Sci, 2020,21:8736.doi:10.3390/ijms21228736.
[15]	Botzenhart UU, Vaal V, Rentzsch I, et al. Changes in caveolin-1, caveolin-3 and vascular endothelial growth factor expression and protein content after botulinum toxin A injection in the right masseter muscle of dystrophin deficient (mdx-) mice[J]. Physiol Pharmacol, 2017,68:181-189.
[16]	Chen X, Zhang J, Wang K. Inhibition of intracellular proton-sensitive Ca2+-permeable TRPV3 channels protects against ischemic brain injury[J]. Acta Pharm Sin B,2022,12:2330-2347.
[17]	Hou X, Huang M, Zeng X, et al. The role of TRPC6 in renal ischemia/reperfusion and cellular hypoxia/reoxygenation injuries[J]. Front Mol Biosci, 2021,8:698975.doi:10.3389/fmolb.2021.698975.
[18]	Ye J, Wang R, Wang M, et al. Hydroxysafflor yellow A ameliorates myocardial ischemia/reperfusion injury by suppressing calcium overload and apoptosis[J]. Oxid Med Cell Longev, 2021,2021:6643615.doi:10.1155/2021/6643615.
[19]	Zheng X, Li J, Fan Q, et al. Dexmedetomidine alleviates myocardial ischemia/reperfusion-induced injury and Ca2+ overload via the microRNA-346-3p/CaMKIId axis[J]. Int J Cardiol,2021,338:185-195.doi:10.1016/j.ijcard.2021.03.016.
[20]	Nesovic Ostojic J, Ivanov M, Mihailovic-Stanojevic N, et al. Hyperbaric oxygen preconditioning upregulates heme oxygenase-1 and anti-apoptotic Bcl-2 protein expression in spontaneously hypertensive rats with induced postischemic acute kidney injury[J]. Int J Mol Sci, 2021,22:1382.doi:10.3390/ijms22031382.
[21]	Wu L, Huang WQ, Yu CC, et al. Moderate hydrogen peroxide postconditioning ameliorates ischemia/reperfusion injury in cardiomyocytes via STAT3-induced calcium, ROS, and ATP homeostasis[J]. Pharmacology,2021,106:275-285.doi:10.1159/000511961.
[22]	Wang R, Wang M, Zhou J, et al. Calenduloside E suppresses calcium overload by promoting the interaction between L-type calcium channels and Bcl2-associated athanogene 3 to alleviate myocardial ischemia/reperfusion injury[J]. Adv Res, 2020,34:173-186.
[23]	Menezes-Rodrigues FS, Tavares JGP, Vasques ER, et al. Cardioprotective effects of pharmacological blockade of the mitochondrial calcium uniporter on myocardial ischemia-reperfusion injury[J].Acta Cir Bras, 2020,35:e202000306.doi:10.1590/s0102-865020200030000006.
[24]	Lin BL, Shin JY, Jeffreys WP, et al. Pharmacological TRPC6 inhibition improves survival and muscle function in mice with Duchenne muscular dystrophy[J]. JCI Insight, 2022,7: e158906. doi:10.1172/jci.insight.158906.