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Updated: Oct 2, 2025
An Effective Mouse Model of Unilateral Renal Ischemia-Reperfusion Injury
Published on: July 15, 2021
Unilateral Acute Renal Ischemia-Reperfusion Injury Induces Cardiac Dysfunction through Intracellular Calcium
Carolina Victoria Cruz Junho1,2, Laura González-Lafuente2, José Alberto Navarro-García2
1Center of Natural and Human Sciences (CCNH), Federal University of ABC, Santo André 09210-580, SP, Brazil.
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 (SERCA2a) 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.
Insights
Renal ischemia-reperfusion injury impairs heart cell function by disrupting calcium handling, leading to contraction problems and arrhythmias that persist long-term.
Area of Science:
- Cardiology
- Nephrology
- Cellular Physiology
Background:
- Acute renal failure (ARF) following renal ischemia-reperfusion (I/R) injury is a known cardiac risk factor.
- Mechanisms of cardiac damage at the cardiomyocyte level post-renal I/R are poorly understood.
Purpose of the Study:
- To investigate the impact of renal I/R injury on intracellular calcium (Ca2+) dynamics in cardiomyocytes.
- To elucidate the long-term effects of renal I/R on cardiomyocyte function and arrhythmogenesis.
Main Methods:
- Adult ventricular cardiomyocytes were isolated from C57BL/6 mice 7 and 15 days after unilateral renal I/R.
- Intracellular Ca2+ dynamics, including Ca2+ transients, SERCA2a activity, and pro-arrhythmic events (Ca2+ sparks, waves), were analyzed.
Main Results:
- Seven days post-I/R, cardiomyocytes exhibited reduced contraction, decreased systolic Ca2+ transients, and impaired SERCA2a activity.
- An increased incidence of pro-arrhythmic Ca2+ events was observed 7 days post-I/R.
- While contraction and systolic Ca2+ transients recovered by 15 days, Ca2+ leak and arrhythmic events remained elevated.
Conclusions:
- Renal I/R injury induces cardiomyocyte Ca2+ cycle dysfunction.
- Contraction-relaxation dysfunction occurs at a medium-term (7 days) post-renal I/R.
- Long-term (15 days) Ca2+ leak and arrhythmogenic potential persist after renal I/R.
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