Osteoarthritis (OA) is a debilitating degenerative disease of the articular cartilage with a multifactorial etiology. Aging, the main risk factor for OA development, is associated with a systemic oxidative and inflammatory phenotype. Autophagy is a central housekeeping system that plays an antiaging role by supporting the clearance of senescence-associated alterations of macromolecules and organelles. Autophagy deficiency has been related to OA pathogenesis because of the accumulation of cellular defects in chondrocytes. Microribonucleic acids (microRNAs or miRs) are a well-established class of posttranscriptional modulators belonging to the family of noncoding RNAs that have been identified as key players in the regulation of cellular processes, such as autophagy, by targeting their own cognate mRNAs. Here, we present a state-of-the-art literature review on the role of miRs and autophagy in the scenario of OA pathogenesis. In addition, a comprehensive survey has been performed on the functional connections of the miR network and the autophagy pathway in OA by using "microRNA," "autophagy," and "osteoarthritis" as key words. Discussion of available evidence sheds light on some aspects that need further investigation in order to reach a more comprehensive view of the potential of this topic in OA.

D'Adamo, S., Cetrullo, S., Minguzzi, M., Silvestri, Y., Borzì, R.M., Flamigni, F. (2017). MicroRNAs and Autophagy: Fine Players in the Control of Chondrocyte Homeostatic Activities in Osteoarthritis. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2017, 1-16 [10.1155/2017/3720128].

MicroRNAs and Autophagy: Fine Players in the Control of Chondrocyte Homeostatic Activities in Osteoarthritis

D'ADAMO, STEFANIA;CETRULLO, SILVIA
;
MINGUZZI, MANUELA;SILVESTRI, YLENIA;FLAMIGNI, FLAVIO
2017

Abstract

Osteoarthritis (OA) is a debilitating degenerative disease of the articular cartilage with a multifactorial etiology. Aging, the main risk factor for OA development, is associated with a systemic oxidative and inflammatory phenotype. Autophagy is a central housekeeping system that plays an antiaging role by supporting the clearance of senescence-associated alterations of macromolecules and organelles. Autophagy deficiency has been related to OA pathogenesis because of the accumulation of cellular defects in chondrocytes. Microribonucleic acids (microRNAs or miRs) are a well-established class of posttranscriptional modulators belonging to the family of noncoding RNAs that have been identified as key players in the regulation of cellular processes, such as autophagy, by targeting their own cognate mRNAs. Here, we present a state-of-the-art literature review on the role of miRs and autophagy in the scenario of OA pathogenesis. In addition, a comprehensive survey has been performed on the functional connections of the miR network and the autophagy pathway in OA by using "microRNA," "autophagy," and "osteoarthritis" as key words. Discussion of available evidence sheds light on some aspects that need further investigation in order to reach a more comprehensive view of the potential of this topic in OA.
2017
D'Adamo, S., Cetrullo, S., Minguzzi, M., Silvestri, Y., Borzì, R.M., Flamigni, F. (2017). MicroRNAs and Autophagy: Fine Players in the Control of Chondrocyte Homeostatic Activities in Osteoarthritis. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2017, 1-16 [10.1155/2017/3720128].
D'Adamo, Stefania; Cetrullo, Silvia; Minguzzi, Manuela; Silvestri, Ylenia; Borzì, Rosa Maria; Flamigni, Flavio
File in questo prodotto:
File Dimensione Formato  
OMCL-3720128.pdf

accesso aperto

Descrizione: full text pdf
Tipo: Versione (PDF) editoriale
Licenza: Licenza per Accesso Aperto. Creative Commons Attribuzione (CCBY)
Dimensione 1.96 MB
Formato Adobe PDF
1.96 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/605214
Citazioni
  • ???jsp.display-item.citation.pmc??? 22
  • Scopus 38
  • ???jsp.display-item.citation.isi??? 37
social impact