The Regulatory Role of Ferroptosis in Bone Homeostasis

Abstract

Ferroptosis is an iron-dependent form of programmed cell death and an important type of biological catabolism. Through the action of divalent iron or ester oxygenase, ferroptosis can induce lipid peroxidation and cell death, regulating a variety of physiological processes. The role of ferroptosis in the modulation of bone homeostasis is a significant topic of interest. Herein, we review and discuss recent studies exploring the mechanisms and functions of ferroptosis in different bone-related cells, including mesenchymal stem cells, osteoblasts, osteoclasts, and osteocytes. The association between ferroptosis and disorders of bone homeostasis is also explored in this review. Overall, we aim to provide a detailed overview of ferroptosis, summarizing recent understanding on its role in regulation of bone physiology and bone disease pathogenesis.

Ferroptosis: A potential target for the intervention of intervertebral disc degeneration

“…In recent years, many new ways of programmed cell death have been reported in studies on IVDD. In contrast to apoptosis, necroptosis, pyroptosis, autophagy, and other types of death procedures, ferroptosis is characterized by the iron-mediated accumulation of lipid peroxides, morphologically manifested as mitochondrial shrinkage, reduction of mitochondrial cristae, and rupture of the mitochondrial outer membrane, and it has been regarded as a new target for the treatment of IVDD ( 3 ).…”

XJB-5-131 protects chondrocytes from ferroptosis to alleviate osteoarthritis progression via restoring Pebp1 expression

“…In addition, the pathological features of OA were degeneration of articular cartilage, hyperplasia of subchondral bone, osteogenesis at the joint edge, inflammation and proliferation of synovial tissue [ 54 ]. In our study, although we have provided microCT data of subchondral bone which is consistent with the pathological alleviation of OA, ferroptosis is related to bone homeostasis [ 55 ], and the specific mechanism of subchondral bone remodeling needs to be further explored.…”

Mesenchymal stem cells and ferroptosis: Clinical opportunities and challenges

“…The regulatory role of MSCs in ameliorating ferroptosis is well documented. For example, MSCs can inhibit lipid peroxidation and reduce ferroptosis in vivo and in vitro [ 50 ], human umbilical cord mesenchymal stem cells (HucMSCs) improve erectile dysfunction in diabetic rats by attenuating ferroptosis [ 51 ], MSCs maintain intracellular glutathione levels by directly or indirectly up-regulating the expression of GPX4 to inhibit ferroptosis in myocardial IRI [ 52 ], and MSCs alleviate post-resuscitation heart and brain damage by inhibiting ferroptosis in a pig model of cardiac arrest [ 49 ].…”