Cardiomyopathy is a progressive and debilitating condition characterized by structural
and functional abnormalities of the myocardium, often leading to impaired cardiac
function, systemic congestion, and organ dysfunction. It affects millions of individuals
worldwide, contributing significantly to morbidity and mortality despite advances in
medical management. The pathophysiology of cardiomyopathy is complex and multifactorial,
involving neurohormonal activation, oxidative stress, inflammation, and adverse cardiac
remodeling. Standard treatments, such as angiotensin-converting enzyme (ACE) inhibitors,
beta-blockers, and diuretics, have been shown to improve symptoms and slow disease
progression; however, the prognosis remains poor for many patients, emphasizing the
urgent need for novel therapeutic strategies.
Melatonin, a neurohormone primarily secreted by the pineal gland, has attracted
considerable interest due to its diverse biological properties. Beyond its role in
regulating circadian rhythms, melatonin exhibits potent antioxidant and anti-inflammatory
effects. It scavenges free radicals, reduces lipid peroxidation, and modulates
inflammatory pathways, thereby protecting mitochondrial function and cellular integrity.
Experimental studies have demonstrated melatonin's ability to mitigate myocardial injury
and improve cardiac function in animal models of cardiomyopathy. Preliminary clinical
studies also suggest that melatonin supplementation may improve endothelial function,
reduce sympathetic overactivity, and enhance overall cardiovascular health .
Mitochondrial dysfunction is a hallmark of cardiomyopathy. Melatonin has been shown to
preserve mitochondrial function by maintaining mitochondrial membrane potential,
preventing the opening of the mitochondrial permeability transition pore, and promoting
mitophagy-the selective removal of damaged mitochondria. These actions help sustain ATP
production and reduce cardiomyocyte apoptosis .
Melatonin's antioxidant capacity extends beyond direct scavenging; melatonin also
upregulates the expression of antioxidant enzymes like superoxide dismutase (SOD),
glutathione peroxidase (GPx), and catalase, while simultaneously inhibiting pro-oxidant
enzymes. This dual mechanism makes it particularly effective in mitigating oxidative
stress, a key contributor to the pathogenesis of numerous diseases, including
cardiovascular disorders, neurodegenerative diseases like Alzheimer's and Parkinson's,
diabetes, and cancer. In cardiovascular diseases, melatonin reduces lipid peroxidation
and preserves mitochondrial function, protecting against ischemia-reperfusion injury. In
neurodegenerative conditions, it minimizes neuronal oxidative damage and supports
synaptic integrity. Furthermore, in diabetes, melatonin helps maintain pancreatic β-cell
function by countering oxidative stress and inflammation. These multifaceted antioxidant
properties make melatonin a promising therapeutic agent in oxidative stress-driven
pathologies Given its safety profile and multifaceted mechanisms of action, melatonin
holds promise as an adjunctive therapy in managing cardiomyopathy. Its ability to target
oxidative stress, inflammation, and mitochondrial dysfunction addresses key pathological
processes underlying the disease
In summary, melatonin exhibits several properties that may be beneficial in the context
of cardiomyopathy. Ongoing research is essential to fully elucidate its therapeutic
potential and to determine optimal dosing strategies for affected patients.