Heart World Conference 2026

Abstract

Background:
Ischemic heart disease remains the leading cause of morbidity and mortality worldwide. Despite advances in cardiovascular care, effective pharmacological therapies specifically targeting ischemia-reperfusion injury remain an unmet clinical need. CIGB-500, a growth hormone secretagogue hexapeptide, has demonstrated promising cardioprotective effects in experimental models of myocardial infarction and cardiomyopathy.

Methods:
The cardioprotective mechanism of CIGB-500 was investigated using a rat model of permanent left anterior descending coronary artery ligation to induce non-reperfused myocardial infarction. Animals were allocated into sham-operated, infarcted saline-treated, and infarcted CIGB-500-treated groups. Treatment was initiated immediately after surgery and continued for seven days. Cardiac function was assessed by echocardiography and histopathology. To characterize mitochondrial molecular responses, proteomic analysis was performed on cardiomyocytes isolated from healthy rats treated with either CIGB-500 or saline for six hours.

Results:
CIGB-500 significantly reduced myocardial necrosis, interstitial fibrosis, and scar formation while improving left ventricular structure and function. Proteomic profiling demonstrated upregulation of proteins involved in fatty acid β-oxidation, mitochondrial bioenergetics, respiratory electron transport, antioxidant defense, and anti-apoptotic pathways. Conversely, proteins associated with cell death, actin cytoskeleton remodeling, myocardial contractility, and Rho GTPase signaling were downregulated. These molecular changes were associated with enhanced endogenous pro-survival signaling, improved mitochondrial metabolic plasticity, and preservation of myocardial integrity.

Conclusion:
CIGB-500 is a promising cardioprotective therapeutic candidate that mitigates structural and functional cardiac damage following myocardial ischemia. Its cardioprotective effects appear to be mediated through mitochondrial metabolic reprogramming, enhanced cellular stress resistance, and preservation of left ventricular function. These findings support further preclinical and clinical investigation of CIGB-500 as a novel strategy for reducing ischemic myocardial injury.

Keywords: Ischemic heart disease, CIGB-500, cardioprotection, myocardial infarction, mitochondria, proteomics, left ventricular function, metabolic reprogramming.