RIP1 Perturbation Induces Chondrocyte Necroptosis and Promotes Osteoarthritis Pathogenesis via Targeting BMP7

Cheng, Jin; Duan, Xin; Fu, Xin; Jiang, Yanfang; Yang, Peng; Cao, Canhui; Li, Qi; Zhang, Jiying; Hu, Xiaoqing; Zhang, Xin; Ao, Yingfang

doi:10.3389/fcell.2021.638382

Cited by 27 publications

(25 citation statements)

References 62 publications

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“…The RIPK1 kinase inhibitor (Nec‐1) could potently prevent the trauma‐induced cartilage degradation and limb pain in rats. 121 Consistent with RIPK1, RIPK3 also plays a crucial role in OA pathogenesis. Jeon et al.…”

Section: Necroptosis In Human Diseases and Animal Modelsmentioning

confidence: 94%

The role of necroptosis in disease and treatment

Liu

Xie

Ren

et al. 2021

MedComm

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Necroptosis, a distinctive type of programmed cell death different from apoptosis or necrosis, triggered by a series of death receptors such as tumor necrosis factor receptor 1 (TNFR1), TNFR2, and Fas. In case that apoptosis process is blocked, necroptosis pathway is initiated with the activation of three key downstream mediators which are receptor‐interacting serine/threonine protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain‐like protein (MLKL). The whole process eventually leads to destruction of the cell membrane integrity, swelling of organelles, and severe inflammation. Over the past decade, necroptosis has been found widely involved in life process of human beings and animals. In this review, we attempt to explore the therapeutic prospects of necroptosis regulators by describing its molecular mechanism and the role it played in pathological condition and tissue homeostasis, and to summarize the research and clinical applications of corresponding regulators including small molecule inhibitors, chemicals, Chinese herbal extracts, and biological agents in the treatment of various diseases.

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Section: Necroptosis In Human Diseases and Animal Modelsmentioning

confidence: 94%

The role of necroptosis in disease and treatment

Liu

Xie

Ren

et al. 2021

MedComm

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“…The role played by inflammatory cell death (both pyroptosis and necroptosis) in OA pathogenesis is well defined. Several studies have reported increased inflammatory cell death during OA progression [48,49]. Phosphorylation of MLKL by the protein kinase RIPK3 induces necroptosis and OA progression [50].…”

Section: Plos Onementioning

confidence: 99%

Coenzyme Q10 encapsulated in micelles ameliorates osteoarthritis by inhibiting inflammatory cell death

Woo

Kim³

et al. 2022

PLoS ONE

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Background Osteoarthritis (OA) is the most common degenerative joint disease and is characterized by breakdown of joint cartilage. Coenzyme Q10 (CoQ10) exerts diverse biological effects on bone and cartilage; observational studies have suggested that CoQ10 may slow OA progression and inflammation. However, any effect of CoQ10 on OA remains unclear. Here, we investigated the therapeutic utility of CoQ10-micelles. Methods Seven-week-old male Wistar rats were injected with monosodium iodoacetate (MIA) to induce OA. CoQ10-micelles were administered orally to MIA-induced OA rats; celecoxib served as the positive control. Pain, tissue destruction, and inflammation were measured. The expression levels of catabolic and inflammatory cell death markers were assayed in CoQ10-micelle-treated chondrocytes. Results Oral supplementation with CoQ10-micelles attenuated OA symptoms remarkably, including pain, tissue destruction, and inflammation. The expression levels of the inflammatory cytokines IL-1β, IL-6, and MMP-13, and of the inflammatory cell death markers RIP1, RIP3, and pMLKL in synovial tissues were significantly reduced by CoQ10-micelle supplementation, suggesting that CoQ10-micelles might attenuate the synovitis of OA. CoQ10-micelle addition to cultured OA chondrocytes reduced the expression levels of catabolic and inflammatory cell death markers. Conclusions CoQ10-micelles might usefully treat OA.

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“…Like necrosis, necroptosis is an inflammatory form of cell death resulting in the release of DAMPs into the extracellular space. DAMPs released via necroptosis have been implicated in the pathogenesis of several diseases, with recent studies identifying potential roles in acute kidney injury [162], osteoarthritis [163] and cardiovascular disease [164].…”

Section: Epithelial Damage and Copdmentioning

confidence: 99%

The Role of Epithelial Damage in the Pulmonary Immune Response

Burgoyne

Fisher

Borthwick

2021

Cells

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Pulmonary epithelial cells are widely considered to be the first line of defence in the lung and are responsible for coordinating the innate immune response to injury and subsequent repair. Consequently, epithelial cells communicate with multiple cell types including immune cells and fibroblasts to promote acute inflammation and normal wound healing in response to damage. However, aberrant epithelial cell death and damage are hallmarks of pulmonary disease, with necrotic cell death and cellular senescence contributing to disease pathogenesis in numerous respiratory diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and coronavirus disease (COVID)-19. In this review, we summarise the literature that demonstrates that epithelial damage plays a pivotal role in the dysregulation of the immune response leading to tissue destruction and abnormal remodelling in several chronic diseases. Specifically, we highlight the role of epithelial-derived damage-associated molecular patterns (DAMPs) and senescence in shaping the immune response and assess their contribution to inflammatory and fibrotic signalling pathways in the lung.

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RIP1 Perturbation Induces Chondrocyte Necroptosis and Promotes Osteoarthritis Pathogenesis via Targeting BMP7

Cited by 27 publications

References 62 publications

The role of necroptosis in disease and treatment

The role of necroptosis in disease and treatment

Coenzyme Q10 encapsulated in micelles ameliorates osteoarthritis by inhibiting inflammatory cell death

The Role of Epithelial Damage in the Pulmonary Immune Response

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