Abstract
Ferroptosis, an instance of iron-dependent programmable cell death that results from oxidative stress & lipid peroxidation, has garnered interest due to its associations with cardiovascular diseases, such as atherosclerosis, myocardial infarction, as well as heart failure. Unlike necrosis or apoptosis, ferroptosis involves unique metabolic pathways that disrupt cellular redox balance and lipid homeostasis, leading to substantial cell damage in cardiovascular tissues. It is becoming recognized that phytoconstituents-bioactive compounds derived from plants-can modify ferroptosis pathways and provide cardioprotective advantages. Compounds including curcumin, resveratrol, quercetin, tanshinone IIA, and epigallocatechin gallate (EGCG) have shown potential in preclinical studies by concentrating on significant ferroptotic processes. Finally, by controlling iron homeostasis, boosting antioxidant responses (such as Nrf2 pathway activation), and reducing lipid peroxidation, these phytochemicals may mitigate ferroptosisinduced cardiac cell death. In animal studies, these natural compounds have shown promise in reducing oxidative damage and improving heart function after injury. This article summarises the mechanisms via which a variety of phytoconstituents influence ferroptosis and discusses their potential as an adjuvant treatment for CVD. While these findings are encouraging, further research is needed to use them in clinical settings, with a focus on long-term safety in human populations, optimal dose, and absorption. The cardioprotective properties of phytoconstituents, which focus on ferroptosis, may provide a unique, plant-based therapeutic strategy for the treatment of CVDs.