Ferroptosis: Implications in Diseases and Potential Treatment Approaches

Komal Kontam R^*, Nivetha M and N Venkateswaramurthy

Department of Pharmacy Practice, JKKN College of Pharmacy, Kumarapalayam, Tamil Nadu, India.

Corresponding Author E-mail: nvmurthi@gmail.com

DOI : http://dx.doi.org/10.13005/bbra/3239

ABSTRACT: Ferroptosis is a recently recognized iron dependent form of regulated cell death. Ferroptotic cells are smaller than normal mitochondria and are usually cristae in structure. Ras-selective lethal small molecule (RSLs) induced cell death is blocked by anti-oxidants and iron chelators. Thus, the term ferroptosis often refers to a non-apoptotic, iron dependent form of regulated cell death (RCD). In 2016, it was found that there are 4 classes of inducers of ferroptosis which includes erastin, glutamate, sorafenib, RSL-3, FIN 56, etc and other reagents like CCL4 and artesunate may induce ferroptosis in liver and pancreatic cancer cells. Age-related and degenerative diseases necessarily cause an increase in brain iron levels, which can be seen in both post-mortem and living samples. Hepatochromatosis and other tissues and illnesses with ferroptosis have both been researched. The presence of ferroptosis is consistent with a variety of clinicopathologic dementia characteristics. Other neurodegenerative illnesses have comparable symptoms. A variety of pharmacological treatment for inhibiting ferroptosis in diseases have been reported like iron chelators, lipophilic antioxidant and β-mercaptoethanol.

KEYWORDS: Apoptosis; Degenerative disease; Erastin;  Ferroptosis; Iron chelators; Regulated cell death

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