Role of Imbalance of Lipid Peroxidation and Articular Cartilage Remodeling in the Pathogenesis of Early Primary and Post-Traumatic Gonarthrosis in Rats

Гладкова, Е. В.

doi:10.1007/s10517-022-05405-6

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…Zubavlenko et al [ 53 ] have observed the activation of the lipid peroxidation process in posttraumatic osteoarthrosis (PTOA) rat models. Moreover, Gladkova et al [ 54 ] also found that increased production of primary and intermediate lipid peroxidation products (hydroxyl radicals, MDA) in PTOA rats. Previous studies have reported that lipid peroxidation has a role in osteoporotic bone loss [ 55 ] and synovial inflammation [ 56 ].…”

Section: Pathological Aspects Of Lipid Peroxidation In Oamentioning

confidence: 99%

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis

Zhang,

Hou,

Guo

et al. 2023

Cell Death Discov.

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Osteoarthritis (OA) is a multifactorial and increasingly prevalent degenerative disease that affects the whole joint. The pathogenesis of OA is poorly understood and there is a lack of therapeutic interventions to reverse the pathological process of this disease. Accumulating studies have shown that the overproduction of reactive oxygen species (ROS) and ROS-induced lipid peroxidation are involved in the pathogenesis of OA. 4-Hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) have received considerable attention for their role in cartilage degeneration and subchondral bone remodeling during OA development. Ferroptosis is a form of cell death characterized by a lack of control of membrane lipid peroxidation and recent studies have suggested that chondrocyte ferroptosis contributes to OA progression. In this review, we aim to discuss lipid peroxidation-derived 4-HNE and MDA in the progression of OA. In addition, the therapeutic potential for OA by controlling the accumulation of lipid peroxidation and inhibiting chondrocyte ferroptosis are discussed.

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Section: Pathological Aspects Of Lipid Peroxidation In Oamentioning

confidence: 99%

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis

Zhang,

Hou,

Guo

et al. 2023

Cell Death Discov.

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“…When cell membrane lipids (phospholipids, glycolipids, and cholesterol) are attacked by ROS, peroxidised lipids produce lipid peroxides, such as MDA, which reacts with DNA or proteins in the body and further damages the composition and structure of the cell membrane (Foret et al, 2019;Ai et al, 2021). Gladkova (Gladkova, 2022) and Zubavlenko et al (Zubavlenko et al, 2021) found that the levels of MDA and lipid peroxides in the serum of an anterior cruciate ligament transection (ACLT) surgery induced OA rat model increased, and the progression of OA could be alleviated by inhibiting the production of MDA and lipid peroxides. GPX4 is a lipid repair enzyme involved in liposome peroxidation, which is regulated by GSH (Ursini and Maiorino, 2020;Wei et al, 2020).…”

Section: Lipid Peroxidation and Osteoarthritismentioning

confidence: 99%

New insight of the pathogenesis in osteoarthritis: the intricate interplay of ferroptosis and autophagy mediated by mitophagy/chaperone-mediated autophagy

An,

Zhang,

Gao

et al. 2023

Front. Cell Dev. Biol.

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Ferroptosis, characterized by iron accumulation and lipid peroxidation, is a form of iron-driven cell death. Mitophagy is a type of selective autophagy, where degradation of damaged mitochondria is the key mechanism for maintaining mitochondrial homeostasis. Additionally, Chaperone-mediated autophagy (CMA) is a biological process that transports individual cytoplasmic proteins to lysosomes for degradation through companion molecules such as heat shock proteins. Research has demonstrated the involvement of ferroptosis, mitophagy, and CMA in the pathological progression of Osteoarthritis (OA). Furthermore, research has indicated a significant correlation between alterations in the expression of reactive oxygen species (ROS), adenosine monophosphate (AMP)-activated protein kinase (AMPK), and hypoxia-inducible factors (HIFs) and the occurrence of OA, particularly in relation to ferroptosis and mitophagy. In light of these findings, our study aims to assess the regulatory functions of ferroptosis and mitophagy/CMA in the pathogenesis of OA. Additionally, we propose a mechanism of crosstalk between ferroptosis and mitophagy, while also examining potential pharmacological interventions for targeted therapy in OA. Ultimately, our research endeavors to offer novel insights and directions for the prevention and treatment of OA.

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“…Goranov et al [ 63 ] and Chang et al [ 64 ] found similar results in the same OA model of dogs and obese rats. Gladkova et al [ 65 ] and Zubavlenko et al [ 66 ] found increased MDA and lipid peroxide levels in the serum of ACLT-induced OA rat models. Bai et al [ 67 ] found increased MDA and decreased GSH levels in the serum of rat models of OA established by DMM compared to control rats.…”

Section: Potential Association Between Ferroptosis and Oa: Animal Modelsmentioning

confidence: 99%

The Role Played by Ferroptosis in Osteoarthritis: Evidence Based on Iron Dyshomeostasis and Lipid Peroxidation

Zhang

et al. 2022

Antioxidants

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Ferroptosis, a recently discovered regulated cell death modality, is characterised by iron-dependent accumulation of lipid hydroperoxides, which can reach lethal levels but can be specifically reversed by ferroptosis inhibitors. Osteoarthritis (OA), the most common degenerative joint disease, is characterised by a complex pathogenesis involving mechanical overload, increased inflammatory mediator levels, metabolic alterations, and cell senescence and death. Since iron accumulation and oxidative stress are the universal pathological features of OA, the role played by ferroptosis in OA has been extensively explored. Increasing evidence has shown that iron dyshomeostasis and lipid peroxidation are closely associated with OA pathogenesis. Therefore, in this review, we summarize recent evidence by focusing on ferroptotic mechanisms and the role played by ferroptosis in OA pathogenesis from the perspectives of clinical findings, animal models, and cell research. By summarizing recent research advances that characterize the relationship between ferroptosis and OA, we highlight avenues for further research and potential therapeutic targets.

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Role of Imbalance of Lipid Peroxidation and Articular Cartilage Remodeling in the Pathogenesis of Early Primary and Post-Traumatic Gonarthrosis in Rats

Cited by 3 publications

References 6 publications

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis

New insight of the pathogenesis in osteoarthritis: the intricate interplay of ferroptosis and autophagy mediated by mitophagy/chaperone-mediated autophagy

The Role Played by Ferroptosis in Osteoarthritis: Evidence Based on Iron Dyshomeostasis and Lipid Peroxidation

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