Ferroptosis: a promising candidate for exosome-mediated regulation in different diseases

Abstract

Ferroptosis is a newly discovered form of cell death that is featured in a wide range of diseases. Exosome therapy is a promising therapeutic option that has attracted much attention due to its low immunogenicity, low toxicity, and ability to penetrate biological barriers. In addition, emerging evidence indicates that exosomes possess the ability to modulate the progression of diverse diseases by regulating ferroptosis in damaged cells. Hence, the mechanism by which cell-derived and noncellular-derived exosomes target ferroptosis in different diseases through the system Xc−/GSH/GPX4 axis, NAD(P)H/FSP1/CoQ10 axis, iron metabolism pathway and lipid metabolism pathway associated with ferroptosis, as well as its applications in liver disease, neurological diseases, lung injury, heart injury, cancer and other diseases, are summarized here. Additionally, the role of exosome-regulated ferroptosis as an emerging repair mechanism for damaged tissues and cells is also discussed, and this is expected to be a promising treatment direction for various diseases in the future.

Ferroptosis in Cancer Therapy: Mechanisms, Small Molecule Inducers, and Novel Approaches

“…The Xc − -GSH-GPX4 axis is a central regulatory pathway for ferroptosis. 34 The Cystine/Glutamate Antiporter (System Xc − ) is on the cytoplasmic membrane. It contains solute carrier family 3 member 2 Gene (SLC3A2) and solute carrier family 7 member 11 Gene (SLC7A11, xCT), which is responsible for the transfer of cysteine(Cys) into the cell and glutamate(Glu) out of the cell.…”

Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis

“…Notably, exosome and ferroptosis may interplay with each other [ 10 , 11 , 12 , 13 , 14 , 15 ]. Exosomes may enhance or suppress ferroptosis in several diseases and cancers [ 16 ]. The inhibition of ferroptosis may be triggered via exosome-mediated regulation that acts on ferroptosis signaling [ 10 ].…”