Focused low-intensity pulsed ultrasound alleviates osteoarthritis via restoring impaired FUNDC1-mediated mitophagy

Ye, Haixia; Li, Dongqian; Wei, Xia; Yu, Lehua; Jia, Lang

doi:10.1016/j.isci.2023.107772

Cited by 6 publications

(1 citation statement)

References 40 publications

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“…Focused low-intensity pulsed ultrasound (FLIPUS) treatment significantly enhanced the protein level of phosphoglycerate mutase 5 (PGAM5) in interleukin-1β (IL-1β)-induced primary mouse chondrocytes of knee joints, promoted Ser13 dephosphorylation containing FUN14 do domain protein 1 (FUNDC1), activated mitophagy in chondrocytes, significantly upregulated the expression of collagen II (Col II) and B-cell lymphoma/leukemia-2 (Bcl-2), downregulated matrix metalloproteinase 13 (MMP13), Bcl-2 associated X protein (Bax), and cleaved caspase-3 expression, and attenuated extracellular matrix (ECM) degradation and apoptosis. In vivo experiments further confirmed that FLIPUS could alleviate ECM loss and chondrocyte apoptosis in a destabilization of the medial meniscus (DMM) mouse model through mitophagy mediated by FUNDC1, thereby exerting a protective effect on cartilage ( Ye et al, 2023 ). In addition, syntaxin 17 (STX17) ( Xu et al, 2023 ), FK506 binding protein 8 (FKBP8) ( Yoo et al, 2020 ), nucleotide-binding domain and leucine-rich repeat-containing family member X1 (NLRX1) ( Zhang Y. et al, 2019 ), prohibitin 2 (PHB2) ( Lai et al, 2023 ), cardiolipin (CL) ( Yang et al, 2023 ), thioredoxin-interacting protein (Txnip) ( Zhang S. et al, 2023 ), dual-specificity protein phosphatase 1 (DUSP1) ( Li R. et al, 2023 ), and other mitophagy-related receptors have also been shown to mediate mitophagy under stress conditions.…”

Section: Overview Of Mitophagymentioning

confidence: 85%

The role of mitophagy in metabolic diseases and its exercise intervention

Tang,

Geng,

Lin

2024

Front. Physiol.

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Mitochondria are energy factories that sustain life activities in the body, and their dysfunction can cause various metabolic diseases that threaten human health. Mitophagy, an essential intracellular mitochondrial quality control mechanism, can maintain cellular and metabolic homeostasis by removing damaged mitochondria and participating in developing metabolic diseases. Research has confirmed that exercise can regulate mitophagy levels, thereby exerting protective metabolic effects in metabolic diseases. This article reviews the role of mitophagy in metabolic diseases, the effects of exercise on mitophagy, and the potential mechanisms of exercise-regulated mitophagy intervention in metabolic diseases, providing new insights for future basic and clinical research on exercise interventions to prevent and treat metabolic diseases.

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Section: Overview Of Mitophagymentioning

confidence: 85%

The role of mitophagy in metabolic diseases and its exercise intervention

Tang,

Geng,

Lin

2024

Front. Physiol.

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Characterization and functional analysis of SOCS9 from orange-spotted grouper (Epinephelus coioides) during virus infection

Chen,

et al. 2024

Fish & Shellfish Immunology

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Low-intensity pulsed ultrasound delays the progression of osteoarthritis by regulating the YAP–RIPK1–NF-κB axis and influencing autophagy

Pan,

Lu,

Hao

et al. 2024

J Transl Med

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Background Osteoarthritis (OA) is a degenerative disease characterized by chronic inflammation of the joint. As the disease progresses, patients will gradually develop symptoms such as pain, physical limitations and even disability. The risk factors for OA include genetics, gender, trauma, obesity, and age. Unfortunately, due to limited understanding of its pathological mechanism, there are currently no effective drugs or treatments to suspend the progression of osteoarthritis. In recent years, some studies found that low-intensity pulsed ultrasound (LIPUS) may have a positive effect on osteoarthritis. Nonetheless, the exact mechanism by which LIPUS affects osteoarthritis remains unknown. It is valuable to explore the specific mechanism of LIPUS in the treatment of OA. Methods In this study, we validated the potential therapeutic effect of LIPUS on osteoarthritis by regulating the YAP–RIPK1–NF-κB axis at both cellular and animal levels. To verify the effect of YAP on OA, the expression of YAP was knocked down or overexpressed by siRNA and plasmid in chondrocytes and adeno-associated virus was injected into the knee joint of rats. The effect of LIPUS was investigated in inflammation chondrocytes induced by IL-1β and in the post-traumatic OA model. Results In this study, we observed that YAP plays an important role in the development of osteoarthritis and knocking down of YAP significantly inhibited the inflammation and alleviated cartilage degeneration. We also demonstrated that the expression of YAP was increased in osteoarthritis chondrocytes and YAP could interact with RIPK1, thereby regulating the NF-κB signal pathway and influencing inflammation. Moreover, we also discovered that LIPUS decreased the expression of YAP by restoring the impaired autophagy capacity and inhibiting the binding between YAP and RIPK1, thereby delaying the progression of osteoarthritis. Animal experiment showed that LIPUS could inhibit cartilage degeneration and alleviate the progression of OA. Conclusions These results showed that LIPUS is effective in inhibiting inflammation and cartilage degeneration and alleviate the progression of OA. As a result, our results provide new insight of mechanism by which LIPUS delays the development of osteoarthritis, offering a novel therapeutic regimen for osteoarthritis.

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Focused low-intensity pulsed ultrasound alleviates osteoarthritis via restoring impaired FUNDC1-mediated mitophagy

Cited by 6 publications

References 40 publications

The role of mitophagy in metabolic diseases and its exercise intervention

The role of mitophagy in metabolic diseases and its exercise intervention

Characterization and functional analysis of SOCS9 from orange-spotted grouper (Epinephelus coioides) during virus infection

Low-intensity pulsed ultrasound delays the progression of osteoarthritis by regulating the YAP–RIPK1–NF-κB axis and influencing autophagy

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