Key result
Overexpression of cyto-renin in cardiac H9c2 cells enhanced aerobic glycolysis and mitochondrial spare capacity, indicating an increased potential to tolerate stress conditions.
Why the study?
Does cyto-renin overexpression improve metabolic and mitochondrial functions in cardiac H9c2 cells?
Does cyto-renin overexpression improve metabolic and mitochondrial functions in cardiac H9c2 cells?
Cyto-renin induces a cardioprotective metabolic switch to aerobic glycolysis and enhances mitochondrial stress tolerance in cardiac cells, highlighting it as a potential target for preventing ischemia-induced myocardial damage.
May support cyto-renin as metabolic target in cardiac cells; leaves open translation to ischemia protection in vivo.
The renin-angiotensin system promotes oxidative stress, apoptosis, necrosis, fibrosis, and thus heart failure. Secretory renin plays a central role in these processes, initiating the generation of angiotensins. Nevertheless, alternative renin transcripts exist, which code for a cytosolically localized renin isoform (cyto-renin) that is cardioprotective. We tested the hypothesis that the protective effects are associated with a beneficial switch of metabolic and mitochondrial functions. To assess H9c2 cell mitochondrial parameters, we used the Seahorse XF analyser. Cardiac H9c2 cells overexpressing cyto-renin exhibited enhanced nonmitochondrial oxygen consumption, lactate accumulation, and LDH activity, reflecting a switch to more aerobic glycolysis known as Warburg effect. Additionally, mitochondrial spare capacity and cell respiratory control ratio were enhanced, indicating an increased potential to tolerate stress conditions. Renin knockdown induced opposite effects on mitochondrial functions without influencing metabolic parameters. Thus, the protective effects of cyto-renin are associated with an altered bioenergetic profile and an enhanced stress tolerance, which are favourable under ischaemic conditions. Therefore, cyto-renin is a promising new target for the prevention of ischaemia-induced myocardial damage.
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Wanka et al. (2018) studied Ischaemia-induced myocardial damage. Cyto-renin overexpression vs. Renin knockdown / control was evaluated on Mitochondrial parameters and metabolic functions. Overexpression of cyto-renin in cardiac H9c2 cells enhanced aerobic glycolysis and mitochondrial spare capacity, indicating an increased potential to tolerate stress conditions.
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