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Ferroptosis: mechanisms and role in diabetes and its complications

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Diabetes mellitus (DM) is a chronic disease mainly characterized by hyperglycemia caused by insufficient insulin secretion and insulin resistance (American Diabetes, 2011, Xu et al., 2018). DM has become an important public health concern worldwide (Serina and Castilho, 2022). The number of adults with DM worldwide is expected to reach 783 million by 2045 (Sun et al., 2022). DM is classified into type 1 DM and type 2 DM (T2DM). Type 1 DM is primarily due to an absolute lack of islet secretion after destruction of islet beta cells, whereas T2DM is primarily due to a progressive insulin secretion defect caused by insulin resistance (American Diabetes , 2015). Without proper control, DM can lead to two serious complications over time: microvascular disease and macrovascular disease. Microangiopathy mainly includes diabetic kidney disease (DKD), diabetic retinopathy (DR), diabetic cardiomyopathy (DCM), diabetic encephalopathy, and diabetic neuropathy; These include cardiovascular disease, diabetic myonecrosis, stroke, and intermittent claudication (Zheng et al., 2021). Ultimately, DM and its complications cause disease in the corresponding organs of patients, which can easily reduce the quality of life and lead to loss of work force. In severe cases, DM and its complications can cause significant physical damage and even be life-threatening. Although the prevention and treatment of DM are constantly being improved with the development of medical science, there is no reliable method to control the occurrence and progression of DM and its complications. Therefore, further exploring the pathological changes and molecular mechanisms of DM and its complications has attracted attention in current research in order to formulate a better treatment plan.

Current forms of controlled cell death (RCD) include apoptosis, necroptosis, autophagy-dependent cell death, pyroptosis, ferroptosis, cuproptosis, etc. (Denton and Kumar, 2019, Mou et al, 2019, Tong et al, 2022). Ferroptosis is an iron-dependent RCD (Dixon et al., 2012, Lei et al., 2021a) (Figure 1) that can be induced by small molecules that inhibit glutathione (GSH) biosynthesis or glutathione peroxidase 4 (GPX4). will be done. and is characterized by iron-dependent accumulation of reactive oxygen species (ROS) and consumption of polyunsaturated fatty acids (PUFA) in cell membranes (Zhou et al., 2020b). In 2012, Dixon et al. (2012) proposed that the term ferroptosis can be used to describe the small molecule elastin-induced cell death that inhibits cystine input and ultimately leads to iron-dependent oxidative death. In the 1950s, Alice Eagle showed that cystine deficiency could cause cell death (Eagle, 1955). Cells undergoing ferroptosis have distinctive morphological characteristics, such as obvious mitochondrial shrinkage, increased membrane density, and reduced or absent mitochondrial cristae (Li et al., 2020b, Tang et al. , 2021a, Yang et al., 2021). Together, these morphological and biochemical features help distinguish ferroptosis from other forms of cell death. Recently, ferroptosis, a type of RCD, has been implicated in the pathological processes of lipid peroxidation and inflammatory activation in various diseases, thereby contributing to the progression of DM and its associated complications. It turns out.

In this review, we will discuss the mechanisms underlying ferroptosis, the relationship of ferroptosis with DM, DKD, DR, DCM, diabetic osteoporosis (DOP), diabetes-associated cognitive dysfunction (DACD), and DM-induced erectile dysfunction (DMED). The purpose was to discuss. and diabetic atherosclerosis (DA). This review can provide research concepts to identify new therapeutic targets and develop new techniques and drugs for the treatment of DM and its complications.

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