Ferroptosis as a Therapeutic Target in Metabolic Syndrome, Mechanism Complications and Future Prospects

Abstract

Metabolic syndrome (MetS) is a risk factor clustering multifactorial disorder, including obesity as experienced in the abdomen, resistance to insulin, dyslipidaemia, high blood pressure, and elevation in level of fasting glucose closely allied with the escalation of the threat of cardiovascular disease, type 2 diabetes, and different related health-related issues. Even though the rate of metabolic syndrome in the world is growing, the current treatment intervention measures have not been sufficient and new measures were desperately needed. The recent studies have emphasized ferroptosis, a regulated cell death process caused by the oxidative stress and lipid peroxidation, as a pathological process of metabolic syndrome. In this paper, the authors examine the processes of ferroptosis, its role in MetS, and its suitability as a therapeutic agent. The prevention of ferroptosis can be a new approach to reducing attacks on the oxidative system, inflammation, and metabolic regulation characteristic of MetS. Nevertheless, there are still difficulties in the interpretation of the exact process of ferroptosis and the creation of efficient and non-toxic inhibitors. Also, ferroptosis inhibition along with other interventions involving insulin resistance, inflammation, and dyslipidaemia could be a more holistic treatment strategy. Further studies are required to realize the therapeutic potential of ferroptosis in MetS and to implement them into clinical practice, which would provide new prospects in the treatment of this increasingly widespread health concern of the population.