Montelukast attenuates interleukin IL-1β-induced oxidative stress and apoptosis in chondrocytes by inhibiting CYSLTR1 (Cysteinyl Leukotriene Receptor 1) and activating KLF2 (Kruppel Like Factor 2)

Li, Zongwei; Wang, Jianming; Ma, Yumin

doi:10.1080/21655979.2021.1984003

Cited by 13 publications

(10 citation statements)

References 34 publications

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“…TERTbutylhydroquinone can effectively prevent oxidative stress and inhibit apoptosis of rat chondrocytes by activating Nrf2 pathway (Yang et al, 2021). Li et al found that montelukast can effectively reduce oxidative stress and apoptosis in chondrocytes and improve the viability of chondrocytes (Li et al, 2021). Transforming growth factor β 1 can protect chondrocytes from oxidative stress by regulating autophagy (Kurakazu et al, 2021).…”

Section: How To Solve the Oxidative Stress In Knee Osteoarthritismentioning

confidence: 99%

The role of oxidative stress in the development of knee osteoarthritis: A comprehensive research review

Liu

Luo²,

Yang³

et al. 2022

Front. Mol. Biosci.

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Knee osteoarthritis (KOA) is one of the most common degenerative diseases, and its core feature is the degeneration and damage of articular cartilage. The cartilage degeneration of KOA is due to the destruction of dynamic balance caused by the activation of chondrocytes by various factors, with oxidative stress playing an important role in the pathogenesis of KOA. The overproduction of reactive oxygen species (ROS) is a result of oxidative stress, which is caused by a redox process that goes awry in the inherent antioxidant defence system of the human body. Superoxide dismutase (SOD) inside and outside chondrocytes plays a key role in regulating ROS in cartilage. Additionally, synovitis is a key factor in the development of KOA. In an inflammatory environment, hypoxia in synovial cells leads to mitochondrial damage, which leads to an increase in ROS levels, which further aggravates synovitis. In addition, oxidative stress significantly accelerates the telomere shortening and ageing of chondrocytes, while ageing promotes the development of KOA, damages the regulation of redox of mitochondria in cartilage, and stimulates ROS production to further aggravate KOA. At present, there are many drugs to regulate the level of ROS, but these drugs still need to be developed and verified in animal models of KOA. We discuss mainly how oxidative stress plays a part in the development of KOA. Although the current research has achieved some results, more research is needed.

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Section: How To Solve the Oxidative Stress In Knee Osteoarthritismentioning

confidence: 99%

The role of oxidative stress in the development of knee osteoarthritis: A comprehensive research review

Liu

Luo²,

Yang³

et al. 2022

Front. Mol. Biosci.

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“…TNF-α and IL-1β are key mediators of inflammatory activation and induction of oxidative stress in FLS and chondrocytes, leading to inflammatory factor secretion, FLS proliferation and invasion, and chondrocyte apoptosis. − After confirming that the nanozyme effectively downregulated the secretion of TNF-α and IL-1β from activated macrophages, we explored whether it could also block the secretion of TNF-α and IL-1β from FLS and chondrocytes. For a start, we verified the uptake of MMV-MnO 2 @DSP in FLS and chondrocytes.…”

Section: Resultsmentioning

confidence: 99%

Messenger Nanozyme for Reprogramming the Microenvironment of Rheumatoid Arthritis

Jia

Ren

Liu

et al. 2022

ACS Appl. Mater. Interfaces

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Dysregulation of superoxide anion (O 2 − ) and hydrogen peroxide (H 2 O 2 ) metabolism in the microenvironment of rheumatoid arthritis (RA) drives the feedback loops of TNF-α and IL-1β thereby inducing an inflammatory storm between immune cells and joint tissue cells. Here, we combine nanoscale manganese dioxide (MnO 2 ) with microvesicles derived from macrophage (MMV). The former possesses superoxide dismutase (SOD) and catalase (CAT)-like activities that can modulate this imbalance, and we amplify the enzyme-like activities by using the amorphous hollow mesoporous structure and surface modification. The latter is a natural endogenous component with the parent cell-like inflammatory homing ability and a unique function of transmitting information to surrounding and distant cells (″messenger function″), which helps amorphous hollow MnO 2 (H−MnO 2 ) nanozymes to cloak in the blood and reach the site of inflammation, where they can not only accumulate in activated macrophages but also pretend to be ″messengers″ that are utilized by fibroblast-like synoviocytes (FLS) and chondrocytes. In addition, we also load dexamethasone sodium phosphate (DSP) for helping the nanozymes work. Messenger nanozyme (MMV-MnO 2 @DSP) inherits the natural properties of MMV and mimics the enzymatic activity of SOD and CAT. It accumulates in activated macrophages to restore the metabolism of O 2 − and H 2 O 2 while promoting repolarization and inhibits the feedback loops of TNF-α and IL-1β among macrophages, fibroblast-like synoviocytes, and chondrocytes, leading to anti-rheumatoid arthritis effects in vitro and in vivo.

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“…The activity of KLF2 was enhanced in the process that montelukast attenuated chondrocyte apoptosis. 94 The role of KLF2 in this process was to reduce the proportion of chondrocyte apoptosis, decrease the expression of pro-apoptotic Bax, APAF-1, Cleaved caspase 3 and Cleaved PARP, and increase the expression of the anti-apoptosis protein B-cell lymphoma 2 (Bcl-2). 94 Similarly, Gao et al found that KLF2 overexpression significantly reduced the percentage of IL-1β-induced apoptosis in SW1353 cells.…”

Section: Klfs and Chondrocyte Apoptosismentioning

confidence: 99%

“…94 The role of KLF2 in this process was to reduce the proportion of chondrocyte apoptosis, decrease the expression of pro-apoptotic Bax, APAF-1, Cleaved caspase 3 and Cleaved PARP, and increase the expression of the anti-apoptosis protein B-cell lymphoma 2 (Bcl-2). 94 Similarly, Gao et al found that KLF2 overexpression significantly reduced the percentage of IL-1β-induced apoptosis in SW1353 cells. Mechanistically, KLF2 overexpression activates Nrf2/ARE signalling to promote the transcription of Nrf2 target genes, thereby inhibiting chondrocyte apoptosis.…”

Section: Klfs and Chondrocyte Apoptosismentioning

confidence: 99%

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KLF transcription factors in bone diseases

Wang,

Han,

Dmitrii

et al. 2024

J Cellular Molecular Medi

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Krüppel‐like factors (KLFs) are crucial in the development of bone disease. They are a family of zinc finger transcription factors that are unusual in containing three highly conserved zinc finger structural domains interacting with DNA. It has been discovered that it engages in various cell functions, including proliferation, apoptosis, autophagy, stemness, invasion and migration, and is crucial for the development of human tissues. In recent years, the role of KLFs in bone physiology and pathology has received adequate attention. In addition to regulating the normal growth and development of the musculoskeletal system, KLFs participate in the pathological process of the bones and joints and are intimately linked to several skeletal illnesses, such as osteoarthritis (OA), rheumatoid arthritis (RA), osteoporosis (OP) and osteosarcoma (OS). Consequently, targeting KLFs has emerged as a promising therapeutic approach for an array of bone disorders. In this review, we summarize the current literature on the importance of KLFs in the emergence and regulation of bone illnesses, with a particular emphasis on the pertinent mechanisms by which KLFs regulate skeletal diseases. We also discuss the need for KLFs‐based medication‐targeted treatment. These endeavours offer new perspectives on the use of KLFs in bone disorders and provide prognostic biomarkers, therapeutic targets and possible drug candidates for bone diseases.

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Montelukast attenuates interleukin IL-1β-induced oxidative stress and apoptosis in chondrocytes by inhibiting CYSLTR1 (Cysteinyl Leukotriene Receptor 1) and activating KLF2 (Kruppel Like Factor 2)

Abstract: Montelukast attenuates interleukin IL-1β-induced oxidative stress and apoptosis in chondrocytes by inhibiting CYSLTR1 (Cysteinyl Leukotriene Receptor 1) and activating KLF2 (Kruppel Like Factor 2

Cited by 13 publications

References 34 publications

The role of oxidative stress in the development of knee osteoarthritis: A comprehensive research review

The role of oxidative stress in the development of knee osteoarthritis: A comprehensive research review

Messenger Nanozyme for Reprogramming the Microenvironment of Rheumatoid Arthritis

KLF transcription factors in bone diseases

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