nilateral Acute Renal Ischemia-Reperfusion Injury Induces Cardiac Dysfunction through Intracellular Calcium Mishandlin

Author(s)

Junho, Carolina Victoria Cruz ^{[1, 2]} ; Gonzalez-Lafuente, Laura ^[2] ; Navarro-Garcia, Jose Alberto ^[2] ; Rodriguez-Sanchez, Elena ^[2] ; Carneiro-Ramos, Marcela Sorelli ^[1] ; Ruiz-Hurtado, Gema ^{[2, 3]}

Affiliation

^[1] Fed Univ ABC, Ctr Nat & Human Sci CCNH, BR-09210580 Santo Andre, SP - Brazil

^[2] Hosp Univ 12 Octubre, Inst Res Imas12, Cardiorenal Translat Lab, Madrid 28041 - Spain

^[3] Hosp Univ 12 Octubre, CIBER CV, Madrid 28041 - Spain

• Document type: Journal article
• Source: NTERNATIONAL JOURNAL OF MOLECULAR SCIENCE; v. 23, n. 4 FEB 2022.
• Web of Science Citations: 0

Abstract

Background: Acute renal failure (ARF) following renal ischemia-reperfusion (I/R) injury is considered a relevant risk factor for cardiac damage, but the underlying mechanisms, particularly those triggered at cardiomyocyte level, are unknown. Methods: We examined intracellular Ca2+ dynamics in adult ventricular cardiomyocytes isolated from C57BL/6 mice 7 or 15 days following unilateral renal I/R. Results: After 7 days of I/R, the cell contraction was significantly lower in cardiomyocytes compared to sham-treated mice. It was accompanied by a significant decrease in both systolic Ca2+ transients and sarco/endoplasmic reticulum Ca2+-ATPase (SERCA(2a)) activity measured as Ca2+ transients decay. Moreover, the incidence of pro-arrhythmic events, measured as the number of Ca2+ sparks, waves or automatic Ca2+ transients, was greater in cardiomyocytes from mice 7 days after I/R than from sham-treated mice. Ca2+ mishandling related to systolic Ca2+ transients and contraction were recovered to sham values 15 days after I/R, but Ca2+ sparks frequency and arrhythmic events remained elevated. Conclusions: Renal I/R injury causes a cardiomyocyte Ca2+ cycle dysfunction at medium (contraction-relaxation dysfunction) and long term (Ca2+ leak), after 7 and 15 days of renal reperfusion, respectively. (AU)

• FAPESP's process: 18/19204-9 - Effects of the silencing and super-expressing of Klotho gene in cardiac function through hypertrophy induced by cardiorenal syndrome
• Grantee: Carolina Victória da Cruz Junho
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate (Direct)
• FAPESP's process: 18/03089-6 - Role of the Klotho/FGF23 axis in the development of Type 3 Cardiorenal Syndrome induced by ischemic renal injury
• Grantee: Carolina Victória da Cruz Junho
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• FAPESP's process: 19/11077-0 - Cardiac alterations induced by renal inflammation models: participation of the Klotho/FGF-23 axis
• Grantee: Marcela Sorelli Carneiro Ramos
• Support Opportunities: Regular Research Grants
• FAPESP's process: 15/19107-5 - TLR4 and complement system : possible key mechanism in renal ischemia/reperfusion induced cardiac hypertrophy
• Grantee: Marcela Sorelli Carneiro Ramos
• Support Opportunities: Regular Research Grants