Ferroptosis Regulated by Hypoxia in Cells

Abstract

Ferroptosis is an oxidative damage-related, iron-dependent regulated cell death with intracellular lipid peroxide accumulation, which is associated with many physiological and pathological processes. It exhibits unique features that are morphologically, biochemically, and immunologically distinct from other regulated cell death forms. Ferroptosis is regulated by iron metabolism, lipid metabolism, anti-oxidant defense systems, as well as various signal pathways. Hypoxia, which is found in a group of physiological and pathological conditions, can affect multiple cellular functions by activation of the hypoxia-inducible factor (HIF) signaling and other mechanisms. Emerging evidence demonstrated that hypoxia regulates ferroptosis in certain cell types and conditions. In this review, we summarize the basic mechanisms and regulations of ferroptosis and hypoxia, as well as the regulation of ferroptosis by hypoxia in physiological and pathological conditions, which may contribute to the numerous diseases therapies.

Liproxstatin‐1 alleviates cartilage degradation by inhibiting chondrocyte ferroptosis in the temporomandibular joint

“…Energy stress‐mediated AMPK signaling inhibits fatty acid synthesis and negatively regulates ferroptosis (Lee et al., 2020). Hypoxia signaling promotes ferroptosis by activating hypoxia‐inducible factors (HIFs) and increasing the production of ROS (Zheng et al., 2023). The induction of chondrocyte ferroptosis increases MMP13 expression while decreasing collagen II expression (Yao et al., 2021).…”