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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
  • Προβολή τεκμηρίου
  •   Ιδρυματικό Αποθετήριο Πανεπιστημίου Θεσσαλίας
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
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Ιδρυματικό Αποθετήριο Πανεπιστημίου Θεσσαλίας
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Understanding the role of chondrocytes in osteoarthritis: utilizing proteomics

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Συγγραφέας
Trachana V., Mourmoura E., Papathanasiou I., Tsezou A.
Ημερομηνία
2019
Γλώσσα
en
DOI
10.1080/14789450.2019.1571918
Λέξη-κλειδί
proteome
proteome
articular cartilage
cartilage explant
cell aging
chondrocyte
human
human cell culture
inflammation
knee meniscus
metabolic disorder
osteoarthritis
pathogenesis
proteomics
Review
secretome
secretory cell
chondrocyte
genetics
metabolism
osteoarthritis
oxidation reduction reaction
pathology
Cellular Senescence
Chondrocytes
Humans
Inflammation
Osteoarthritis
Oxidation-Reduction
Proteome
Proteomics
Taylor and Francis Ltd
Εμφάνιση Μεταδεδομένων
Επιτομή
Introduction: Proteomic analyses have been acknowledged to carry a significant prospective in elucidating the pathogenesis of several diseases, including osteoarthritis (OA). But it has not been an easy road: major technical issues, mainly derived from the complex and rigid nature of the cartilage tissue, had to be faced; an obstacle that led to the development of different approaches. Areas covered: In this review, we categorized the proteomic studies undertaken (proteomic analyses of the cartilage, cartilage explants, cultured chondrocytes, and chondrocytes’ secretome) as part of the different strategies developed in order to overcome tissue and disease-specific challenges. Essentially these approaches aimed at identifying differences in the proteome of healthy vs diseased tissue. Our aim was to point out the novel players that have emerged from these analyses and highlight the associated mechanism(s) suggested to play a role in the pathogenesis of OA. Expert commentary: The identified factors indicate the implication of age-associated mechanisms, such as metabolic deregulation, inflammation, and redox imbalance, in OA onset and/or progression. Taken together these results outline the causal network of the disease and place chondrocytes’ senescence at the center of the emerging aetiopathological atlas. © 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group.
URI
http://hdl.handle.net/11615/79754
Collections
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]

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