ReviewExperimental and therapeutic medicine2018
Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease.
Review in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Bone marrow mesenchymal stem cell exosome-derived miR-223 regulated cellular pyroptosis of macrophage in osteomyelitis through regulating LACC1.Scientific reports · 2025Article
- The Status of Selenium and Zinc in the Urine of Children From Endemic Areas of Kashin-Beck Disease Over Three Consecutive Years.Frontiers in nutrition · 2022Article
- Hypoxia, oxidative stress, and immune evasion: a trinity of the trichothecenes T-2 toxin and deoxynivalenol (DON).Archives of toxicology · 2021Review
- Comparison of the major cell populations among osteoarthritis, Kashin-Beck disease and healthy chondrocytes by single-cell RNA-seq analysis.Cell death & disease · 2021Article
- Bone marrow stromal cells-derived exosomes target DAB2IP to induce microglial cell autophagy, a new strategy for neural stem cell transplantation in brain injury.Experimental and therapeutic medicine · 2020Article
- Exosomes in Food: Health Benefits and Clinical Relevance in Diseases.Advances in nutrition (Bethesda, Md.) · 2020Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have identified a close association between diet and the prevalence of Kashin-Beck disease (KBD); however, the mechanisms via which the diet protects against KBD-associated cartilage injury has remained elusive. Recent international research studies have revealed a therapeutic role of dietary exosome micro (mi)RNAs in repairing chondrocyte lesions by regulating genes and proteins associated with cellular apoptosis and extracellular matrix. Vital molecules affecting bio-functions of chondrocytes, including miR-23b and protein kinase cyclic AMP-activated catalytic subunit β, were preliminarily identified to be dysregulated in cells and cartilage tissue of KBD patients. The function of dietary exosome in the repair of chondrocyte lesions in KBD is a novel topic in this field. It is worth exploring the protective role of dietary exosome-miR-23b against chondrocyte damage through the regulation of the protein kinase A (PKA) signaling pathway. The following aims are significant in future studies: i) To verify the association between exosome and cartilage damage in KBD patients; ii) to identify whether the protective mechanism of miR-23b in cartilage damage proceeds through regulating the PKA pathway; and iii) to explore the therapeutic role of dietary exosome-miR-23b in repairing chondrocyte lesions induced by environmental risk factors. These ideas may help establish the therapeutic role and mechanisms of dietary exosome-miR-23b in repairing chondrocyte lesions at the molecular, cellular and organismal level. These studies may simultaneously elucidate the disease pathogenesis and provide evidence for novel biomarkers and therapeutic methods for KBD.
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