Targeting Cell Death: Pyroptosis, Ferroptosis, Apoptosis and Necroptosis in Osteoarthritis

Yang, Jian; Hu, Shasha; Bian, Yangyang; Yao, Jiangling; Wang, Dong; Liu, Xiaoqian; Guo, Zhiliang; Zhang, Siyuan; Lei, Peng

doi:10.3389/fcell.2021.789948

Cited by 132 publications

(109 citation statements)

References 207 publications

(207 reference statements)

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“…Recent studies on aging-related diseases have indicated that ferroptosis contributes in the pathogenesis of Alzheimer's disease (230-232), Parkinson's disease (233,234), Huntington's disease (235), Depression (236-238), Osteoarthritis (239), Myocardial ischemia and reperfusion (MI/R) (240)(241)(242), Atherosclerosis (243, 244), and Diabetes (245,246). Notably, quercetin shows iron-chelating activity and effectively decrease iron deposition in the hearts, kidneys and liver of iron-dextran-overloaded mice (247), and protects bone marrow-derived mesenchymal stem cells from erastin-induced ferroptosis through antioxidant pathway (248).…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

et al. 2022

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Quercetin, a naturally non-toxic flavonoid within the safe dose range with antioxidant, anti-apoptotic and anti-inflammatory properties, plays an important role in the treatment of aging-related diseases. Sirtuin 1 (SIRT1), a member of NAD+-dependent deacetylase enzyme family, is extensively explored as a potential therapeutic target for attenuating aging-induced disorders. SIRT1 possess beneficial effects against aging-related diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Depression, Osteoporosis, Myocardial ischemia (M/I) and reperfusion (MI/R), Atherosclerosis (AS), and Diabetes. Previous studies have reported that aging increases tissue susceptibility, whereas, SIRT1 regulates cellular senescence and multiple aging-related cellular processes, including SIRT1/Keap1/Nrf2/HO-1 and SIRTI/PI3K/Akt/GSK-3β mediated oxidative stress, SIRT1/NF-κB and SIRT1/NLRP3 regulated inflammatory response, SIRT1/PGC1α/eIF2α/ATF4/CHOP and SIRT1/PKD1/CREB controlled phosphorylation, SIRT1-PINK1-Parkin mediated mitochondrial damage, SIRT1/FoxO mediated autophagy, and SIRT1/FoxG1/CREB/BDNF/Trkβ-catenin mediated neuroprotective effects. In this review, we summarized the role of SIRT1 in the improvement of the attenuation effect of quercetin on aging-related diseases and the relationship between relevant signaling pathways regulated by SIRT1. Moreover, the functional regulation of quercetin in aging-related markers such as oxidative stress, inflammatory response, mitochondrial function, autophagy and apoptosis through SIRT1 was discussed. Finally, the prospects of an extracellular vesicles (EVs) as quercetin loading and delivery, and SIRT1-mediated EVs as signal carriers for treating aging-related diseases, as well as discussed the ferroptosis alleviation effects of quercetin to protect against aging-related disease via activating SIRT1. Generally, SIRT1 may serve as a promising therapeutic target in the treatment of aging-related diseases via inhibiting oxidative stress, reducing inflammatory responses, and restoring mitochondrial dysfunction.

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Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

et al. 2022

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“…As an independent form of cell death, ferroptosis can be clearly distinguished from other forms of cell death by the accumulation of lethal reactive oxygen species (ROS) and lipid peroxidation products caused by iron-dependent reactions ( Table 1 ; Dixon et al, 2012 ; Wu et al, 2012 ; Liu and Levine, 2015 ; Chen et al, 2016 ; Xie et al, 2016 ; Galluzzi et al, 2017 ; D’Arcy, 2019 ; Xu et al, 2019 ; Demarco et al, 2020 ; Mizushima and Levine, 2020 ; Nah et al, 2020 ; Khan et al, 2021 ; Li et al, 2021 ; Nadeem et al, 2021 ; Yang et al, 2021 ; Braicu et al, 2022 ; Lei et al, 2022 ). Ultrastructural changes in mitochondria are the most prominent morphological features of ferroptotic cells.…”

Section: The Process and Regulation Of Ferroptosismentioning

confidence: 99%

Mechanisms of Ferroptosis and Emerging Links to the Pathology of Neurodegenerative Diseases

Sun

Xia

Basnet

et al. 2022

Front. Aging Neurosci.

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Neurodegenerative diseases are a diverse class of diseases attributed to chronic progressive neuronal degeneration and synaptic loss in the brain and/or spinal cord, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis and multiple sclerosis. The pathogenesis of neurodegenerative diseases is complex and diverse, often involving mitochondrial dysfunction, neuroinflammation, and epigenetic changes. However, the pathogenesis of neurodegenerative diseases has not been fully elucidated. Recently, accumulating evidence revealed that ferroptosis, a newly discovered iron-dependent and lipid peroxidation-driven type of programmed cell death, provides another explanation for the occurrence and progression of neurodegenerative diseases. Here, we provide an overview of the process and regulation mechanisms of ferroptosis, and summarize current research progresses that support the contribution of ferroptosis to the pathogenesis of neurodegenerative diseases. A comprehensive understanding of the emerging roles of ferroptosis in neurodegenerative diseases will shed light on the development of novel therapeutic technologies and strategies for slowing down the progression of these diseases.

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“…The regulation of chondrocyte survival is important for the maintenance of proper cartilage structure and function. Apoptosis is an active, physiological process of cell death, playing a critical role in retaining the homeostasis of tissues and cells [ 34 ]; it is regulated by various genes, such as those of the BCL-2 family, identified as controllers and inductors of this mechanism [ 35 ]. Dysregulation of apoptosis is, thus, associated with a variety of diseases including inflammatory and degenerative disorders such as OA and RA [ 35 , 36 ].…”

Section: Discussionmentioning

confidence: 99%

Synovial Fluid Regulates the Gene Expression of a Pattern of microRNA via the NF-κB Pathway: An In Vitro Study on Human Osteoarthritic Chondrocytes

Cheleschi

Tenti

Lorenzini

et al. 2022

IJMS

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Synovial fluid (SF) represents the primary source of nutrients of articular cartilage and is implicated in maintaining cartilage metabolism. We investigated the effects of SF, from patients with osteoarthritis (OA), rheumatoid arthritis (RA), and controls, on a pattern of microRNA (miRNA) in human OA chondrocytes. Cells were stimulated with 50% or 100% SF for 24 h and 48 h. Apoptosis and superoxide anion production were detected by cytometry; miRNA (34a, 146a, 155, 181a), cytokines, metalloproteinases (MMPs), type II collagen (Col2a1), antioxidant enzymes, B-cell lymphoma (BCL)2, and nuclear factor (NF)-κB by real-time PCR. The implication of the NF-κB pathway was assessed by the use of NF-κB inhibitor (BAY-11-7082). RA and OA SF up-regulated miR-34a, -146a, -155, -181a, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, MMP-1, MMP-13, and ADAMTs-5 gene expression, while it down-regulated Col2a1. Pathological SF also induced apoptosis, reduced viability, and decreased BCL2 mRNA, whereas it increased superoxide anions, the expression of antioxidant enzymes, p65 and p50 NF-κB. Opposite and positive results were obtained with 100% control SF. Pre-incubation with BAY-11-7082 counteracted SF effects on miRNA. We highlight the role of the SF microenvironment in regulating some miRNA involved in inflammation and cartilage degradation during OA and RA, via the NF-κB pathway.

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Targeting Cell Death: Pyroptosis, Ferroptosis, Apoptosis and Necroptosis in Osteoarthritis

Cited by 132 publications

References 207 publications

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

Mechanisms of Ferroptosis and Emerging Links to the Pathology of Neurodegenerative Diseases

Synovial Fluid Regulates the Gene Expression of a Pattern of microRNA via the NF-κB Pathway: An In Vitro Study on Human Osteoarthritic Chondrocytes

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