Key result
Targeting ferroptosis emerges as a promising therapeutic strategy for coronary heart disease.
Answers are grounded in this paper and cite their sources.
Reveals the mechanistic links between disordered iron metabolism, ferroptosis, and coronary heart disease, suggesting ferroptosis inhibition as a promising therapeutic strategy.
Coronary heart disease (CHD) is closely related to oxidative stress and inflammatory response and is the most common cardiovascular disease (CVD). Iron is an essential mineral that participates in many physiological and biochemical reactions in the human body. Meanwhile, on the negative side, iron has an active redox capacity, which leads to the accumulation of reactive oxygen species (ROS) and lipid peroxidation. There is growing evidence that disordered iron metabolism is involved in CHD's pathological progression. And the result of disordered iron metabolism is associated with iron overload-induced programmed cell death, often called ferroptosis. That features iron-dependent lipid peroxidation. Ferroptosis may play a crucial role in the development of CHD, and targeting ferroptosis may be a promising option for treating CHD. Here, we review the mechanisms of iron metabolism in cardiomyocytes (CMs) and explain the correlation between iron metabolism and ferroptosis. Meanwhile, we highlight the specific roles of iron metabolism and ferroptosis in the main pathological progression of CHD.
No takes yet. Share an insight, caveat, or question.
Fan et al. (2022) conducted a review in Coronary heart disease. Disordered iron metabolism and ferroptosis was evaluated. Disordered iron metabolism and ferroptosis play a crucial role in the pathological progression of coronary heart disease, suggesting that targeting ferroptosis may be a promising therapeutic option.
Synapse has enriched 10 related papers. Consider them for comparative context: