Selected Publications
Li A, Yi J, Li X and Zhou J. Physiological Ca2+ Transients Versus Pathological Steady-State Ca2+ Elevation, Who Flips the ROS Coin in Skeletal Muscle Mitochondria. Front. Physiol. 2020
https://doi.org/10.3389/fphys.2020.595800
Zhou X, Park KH, Yamazaki D, Lin PH, Nishi M, Ma Z, Qiu L, Murayama T, Zou X, Takeshima H, Zhou J, Ma J. (2020). TRIC-A Channel Maintains Store Calcium Handling by Interacting With Type 2 Ryanodine Receptor in Cardiac Muscle. Circ Res. 14;126(4):417-435.
doi: 10.1161/CIRCRESAHA.119.316241.
Bian Z, Wang Q, Zhou X, Tan T, Park KH, Kramer HF, McDougal A, Laping NJ, Kumar S, Adesanya TMA, Sermersheim M, Yi F, Wang X, Wu J, Gumpper K, Jiang Q, He D, Lin PH, Li H, Guan F, Zhou J, Kohr MJ, Zeng C, Zhu H, Ma J. (2019). Sustained elevation of MG53 in the bloodstream increases tissue regenerative capacity without compromising metabolic function. Nat Commun. 10(1):4659.
doi: 10.1038/s41467-019-12483-0.
Zhou J, Li A, Li X and Yi J. (2019). Dysregulated mitochondrial Ca2+ and ROS signaling in skeletal muscle of ALS mouse model. Arch Biochem Biophys. 663:249-258.
doi: 10.1016/j.abb.2019.01.024. Epub 2019 Jan 22.
Xiao Y, Karam C, Yi J, Zhang L, Li X, Yoon D, Wang H, Dhakal K, Ramlow P, Yu T, Mo Z, Ma J and Zhou J. (2018) ROS-related Mitochondrial Dysfunction in Skeletal Muscle of an ALS Mouse Model during the Disease Progression. Pharmacological Research. pii: S1043-6618(18)30253-6.
doi: 10.1016/j.phrs.2018.09.008.
Kitase Y, Vallejo JA, Gutheil W, Vemula H, Jähn K, Yi J, Zhou J, Brotto M, Bonewald LF. (2018). β-aminoisobutyric acid, L-BAIBA, is a muscle-derived osteocyte survival factor. Cell Report. 22(6):1531-1544.
doi: 10.1016/j.celrep.2018.01.041. PMID: 29425508
Wang H, Yi J, Li X, Xiao Y, Dhakal K, Zhou J. (2018). ALS-associated mutation SOD1G93A leads to abnormal mitochondrial dynamics in osteocytes. Bone. 106:126-138.
doi: 10.1016/j.bone.2017.10.010. PMID: 29030231Chen K, Xu Z, Liu Y, Wang Z, Li Y, Xu X,
Chen C, Xia T, Liao Q, Yao Y, Zeng C, He D, Yang Y, Tan T, Yi J, Zhou J, Zhu H, Ma J, Zeng C. (2017). Irisin protects mitochondria function during pulmonary ischemia/reperfusion injury. Science Translational Medicine. 9(418), eaao6298;
doi: 10.1126/scitranslmed. aao6298
Karam C, Yi J, Dhakal K, Xiao Y, Li X, Mano C, Xu J, Li K, Cheng H, Ma J and Zhou J. (2017). Absence of physiological Ca2+ transients is an initial trigger for mitochondrial dysfunction following denervation in skeletal muscle. Skeletal muscl. 10;7(1):6.
doi: 10.1186/s13395-017-0123-0.
Zhang YG, Wu S, Yi J, Xia Y, Jin D, Zhou J, Sun J. (2017). Target Intestinal Microbiota to Alleviate Disease Progression in Amyotrophic Lateral Sclerosis. Clin Ther. pii: S0149-2918(16)30927-4.
doi: 10.1016/j.clinthera.2016.12.014; PMID: 28129947.
Zhou J and Sun J. (2015). Does the gut drive amyotrophic lateral sclerosis progress? Future Medicine/ Neurodegener Dis Manag. 5(5):375-8.
doi: 10.2217/nmt.15.38.
Zhou J, Yi J, Bonewald L. (2015). Muscle-Bone Crosstalk in Amyotrophic Lateral Sclerosis. Curr Osteoporos Rep. 13(5):274-9.
Wu S, Yi J, Zhang YG, Zhou J* and Sun J*. Leaky intestine and impaired microbiome in an amyotrophic lateral sclerosis mouse model. (2015). Physiological Report. 3(4), e12356. PMID: 25847918.
Zhu K, Yi J, Xiao Y, Lai Y, Song P, Zheng W, Jiao H, Fan J, Wu C, Chen d, Zhou J* and Xiao G*. (2015). Impaired Bone Homeostasis in Amyotrophic Lateral Sclerosis Mice with Muscle Atrophy. J Biol Chem. 27:290 (13): 8081-94.
Xiao Y, Ma C, Yi J, Wu S, Luo G, Xu X, Lin P-H, Sun J and Zhou J. (2015). Suppressed Autophagy Flux in Skeletal Muscle of an Amyotrophic Lateral Sclerosis Mouse Model during Disease Progression. Physiology Report. 3(1) e12271,
doi:10.14814/phys2.12271
Luo G, Yi J, Ma C, Xiao Y, Yi F, Yu T and Zhou J. (2013). Defective mitochondrial dynamics is an early event in skeletal muscle of an amyotrophic lateral sclerosis mouse model. PLoS One. 8(12):e82112.
doi: 10.1371/journal. pone.0082112.
Yi J, Ma C, Li Y, Weisleder N, Ríos E, Ma J, Zhou J. (2011). Mitochondrial Calcium Uptake Regulates Rapid Calcium Transients in Skeletal Muscle during Excitation-Contraction (E-C) Coupling. J Biol Chem. 286:32436-43.
Fang H, Chen M, Ding Y, Shang W, Xu J, Zhang X, Zhang W, Li K, Xiao Y, Gao F, Shang S, Li J-C, Tian X-L, Wang S-Q, Zhou J, Weisleder N, Ma J, Ouyang K, Chen J, Wang X, Zheng M, Wang W, Zhang X, Cheng H. (2011). Imaging superoxide flash and metabolism-coupled mitochondrial permeability transition in living animals. Cell Research (2011):1-10.
Zhou J, Yi J, Fu R, Liu R, Siddique T, Ríos E, Deng HX. (2010). Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis. J Biol Chem. 285: 705-712.
Pouvreau S, Royer L, Yi J, Brum G, Meissner G, Ríos E, and Zhou J. (2007). Voltage-operated Ca2+sparks require isoform 3 RyR channels in muscle. Proc Natl Acad Sci U S A. 104:5235-5240.
Zhou J, Yi J, Royer L, Launikonis BS, González A, García J, and Ríos E. (2006). A probable role of dihydropyridine receptors in repression of Ca2+ sparks, demonstrated in cultured mammalian muscle. Am J Physiol Cell Physiol. 290:C549-C553.
Wang X, Weisleder N, Collet C, Zhou J, Chu Y, Hirata Y, Zhao X, Pan Z, Brotto M, Cheng H, Ma J. (2005). Uncontrolled calcium sparks act as a dystrophic signal for mammalian skeletal muscle. Nature Cell Biology. 7(5):525-30.
Zhou J, Brum G, Gonzalez A, Launikonis BB, Stern MD, Rios E. (2003). Ca2+ sparks and embers of mammalian muscle. Properties of the source. J. Gen. Physiol. 122 (1): 95-114.
Zhou J, Shin HG, Yi J, Shen W, Williams CM, and Murray KT. (2002). Phosphorylation and putative ER retention signals are required for protein kinase A-mediated potentiation of cardiac sodium current. Circ. Res. 91: 540-546.
