Biomarkers of Chondrocyte Apoptosis and Autophagy in Osteoarthritis

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  • Giuseppe Musumeci
    Department of Biomedical and Biotechnological Sciences, Human Anatomy and Histology Section, School of Medicine, University of Catania, Catania 95123, Italy
  • Paola Castrogiovanni
    Department of Biomedical and Biotechnological Sciences, Human Anatomy and Histology Section, School of Medicine, University of Catania, Catania 95123, Italy
  • Francesca Trovato
    Department of Clinical and Experimental Medicine, Internal Medicine Division, School of Medicine, University of Catania, Catania 95123, Italy
  • Annelie Weinberg
    Department of Orthopaedic Surgery, Medical University of Graz, 8036 Graz, Austria
  • Mohammad Al-Wasiyah
    Aziziah Maternity and Children's Hospital, Jeddah 50204, Saudi Arabia
  • Mohammed Alqahtani
    Aziziah Maternity and Children's Hospital, Jeddah 50204, Saudi Arabia
  • Ali Mobasheri
    King Fahd Medical Research Center (KFMRC), King AbdulAziz University, Jeddah 21589, Saudi Arabia

説明

<jats:p>Cell death with morphological and molecular features of apoptosis has been detected in osteoarthritic (OA) cartilage, which suggests a key role for chondrocyte death/survival in the pathogenesis of OA. Identification of biomarkers of chondrocyte apoptosis may facilitate the development of novel therapies that may eliminate the cause or, at least, slow down the degenerative processes in OA. The aim of this review was to explore the molecular markers and signals that induce chondrocyte apoptosis in OA. A literature search was conducted in PubMed, Scopus, Web of Science and Google Scholar using the keywords chondrocyte death, apoptosis, osteoarthritis, autophagy and biomarker. Several molecules considered to be markers of chondrocyte apoptosis will be discussed in this brief review. Molecular markers and signalling pathways associated with chondroycte apoptosis may turn out to be therapeutic targets in OA and approaches aimed at neutralizing apoptosis-inducing molecules may at least delay the progression of cartilage degeneration in OA.</jats:p>

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