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ATPase Inhibitory Factor-1 Disrupts Mitochondrial Ca2+ Handling and Promotes Pathological Cardiac Hypertrophy through CaMKIIδ.
Pavez-Giani MG, Sánchez-Aguilera PI, Bomer N, Miyamoto S, Booij HG, Giraldo P, Oberdorf-Maass SU, Nijholt KT, Yurista SR, Milting H, van der Meer P, Boer RA, Heller Brown J, Sillje HWH, Westenbrink BD. Pavez-Giani MG, et al. Among authors: miyamoto s. Int J Mol Sci. 2021 Apr 23;22(9):4427. doi: 10.3390/ijms22094427. Int J Mol Sci. 2021. PMID: 33922643 Free PMC article.
Mitochondrial reprogramming induced by CaMKIIδ mediates hypertrophy decompensation.
Westenbrink BD, Ling H, Divakaruni AS, Gray CB, Zambon AC, Dalton ND, Peterson KL, Gu Y, Matkovich SJ, Murphy AN, Miyamoto S, Dorn GW 2nd, Heller Brown J. Westenbrink BD, et al. Among authors: miyamoto s. Circ Res. 2015 Feb 27;116(5):e28-39. doi: 10.1161/CIRCRESAHA.116.304682. Epub 2015 Jan 20. Circ Res. 2015. PMID: 25605649 Free PMC article.
Inflammation and NLRP3 Inflammasome Activation Initiated in Response to Pressure Overload by Ca2+/Calmodulin-Dependent Protein Kinase II δ Signaling in Cardiomyocytes Are Essential for Adverse Cardiac Remodeling.
Suetomi T, Willeford A, Brand CS, Cho Y, Ross RS, Miyamoto S, Brown JH. Suetomi T, et al. Among authors: miyamoto s. Circulation. 2018 Nov 27;138(22):2530-2544. doi: 10.1161/CIRCULATIONAHA.118.034621. Circulation. 2018. PMID: 30571348 Free PMC article.
3,283 results