Key result
Trimetazidine treats heart failure in mice by restoring potassium homeostasis and increasing ATP supply.
Why the study?
Intracellular potassium ion homeostasis is crucial for myocardial function and disrupted in heart failure, prompting investigation into whether trimetazidine exerts protective effects on this process.
Does trimetazidine improve K+ homeostasis in myocardial tissue in mice with heart failure?
Does trimetazidine improve K+ homeostasis in myocardial tissue in mice with heart failure?
Trimetazidine exerts protective effects in a murine heart failure model by restoring myocardial potassium ion homeostasis and improving mitochondrial energy metabolism.
Trimetazidine merits human trials in heart failure; leaves open whether potassium homeostasis benefits translate clinically.
The occurrence of heart failure (HF) is closely correlated with the disturbance of mitochondrial energy metabolism, and trimetazidine (TMZ) has been regarded as an effective agent in treating HF. Intracellular potassium ion (K + ) homeostasis, which is modulated by K + channels and transporters, is crucial for maintaining normal myocardial function and can be disrupted by HF. This study is aimed at exploring the protective effect of TMZ on K + homeostasis within myocardial tissue in mice with HF. We observed the pathological changes of myocardial tissue under microscopes and further measured the content of adenosine triphosphate (ATP), the activity of Na + ‐K + ATPase, and the expression of ATP1 α 1 at the mRNA and protein levels. Moreover, we also analyzed the changes in K + flux across the myocardial tissue in mice. As a result, we found that there was a large amount of myocardial fiber lysis and fracture in HF myocardial tissue. Meanwhile, the potassium flux of mice with HF was reduced, and the expression of ATP1 α 1, the activity of Na + ‐K + ATPase, and the supply and delivery of ATP were also decreased. In contrast, TMZ can effectively treat HF by restoring K + homeostasis in the local microenvironment of myocardial tissues.
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Yang et al. (2022) studied Heart failure. Trimetazidine (TMZ) was evaluated on Potassium ion homeostasis, ATP content, Na+-K+ ATPase activity, and ATP1 α 1 expression. Trimetazidine effectively treated heart failure in mice by restoring potassium ion homeostasis, increasing ATP supply, and improving Na+-K+ ATPase activity in myocardial tissues.
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