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  4. Hypoxia Inducible Factor-1α in Osteochondral Tissue Engineering.
 
  • Détails
Titre

Hypoxia Inducible Factor-1α in Osteochondral Tissue Engineering.

Type
article
Institution
Externe
Périodique
Tissue Engineering Part B: Reviews  
Auteur(s)
Taheem, D.K.
Auteure/Auteur
Jell, G.
Auteure/Auteur
Gentleman, E.
Auteure/Auteur
Liens vers les personnes
Gentleman, Eileen  
ISSN
1937-3376
Statut éditorial
Publié
Date de publication
2020-04
Volume
26
Numéro
2
Première page
105
Dernière page/numéro d’article
115
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
Damage to osteochondral (OC) tissues can lead to pain, loss of motility, and progress to osteoarthritis. Tissue engineering approaches offer the possibility of replacing damaged tissues and restoring joint function; however, replicating the spatial and functional heterogeneity of native OC tissue remains a pressing challenge. Chondrocytes in healthy cartilage exist in relatively low-oxygen conditions, while osteoblasts in the underlying bone experience higher oxygen pressures. Such oxygen gradients also exist in the limb bud, where they influence OC tissue development. The cellular response to these spatial variations in oxygen pressure, which is mediated by the hypoxia inducible factor (HIF) pathway, plays a central role in regulating osteo- and chondrogenesis by directing progenitor cell differentiation and promoting and maintaining appropriate extracellular matrix production. Understanding the role of the HIF pathway in OC tissue development may enable new approaches to engineer OC tissue. In this review, we discuss strategies to spatially and temporarily regulate the HIF pathway in progenitor cells to create functional OC tissue for regenerative therapies. Impact statement Strategies to engineer osteochondral (OC) tissue are limited by the complex and varying microenvironmental conditions in native bone and cartilage. Indeed, native cartilage experiences low-oxygen conditions, while the underlying bone is relatively normoxic. The cellular response to these low-oxygen conditions, which is mediated through the hypoxia inducible factor (HIF) pathway, is known to promote and maintain the chondrocyte phenotype. By using tissue engineering scaffolds to spatially and temporally harness the HIF pathway, it may be possible to improve OC tissue engineering strategies for the regeneration of damaged cartilage and its underlying subchondral bone.
Sujets

Animals

Cell- and Tissue-Base...

Chondrocytes/cytology...

Chondrocytes/metaboli...

Chondrogenesis

Humans

Hypoxia-Inducible Fac...

Osteoarthritis/metabo...

Osteoarthritis/pathol...

Osteoarthritis/therap...

Osteoblasts/cytology

Osteoblasts/metabolis...

Osteogenesis

Tissue Engineering/me...

Tissue Scaffolds

HIF-1α

cartilage

hypoxia

osteochondral tissue ...

PID Serval
serval:BIB_E2EF76638E3E
DOI
10.1089/ten.TEB.2019.0283
PMID
31774026
WOS
000506452700001
Permalien
https://iris.unil.ch/handle/iris/250047
Open Access
Oui
Date de création
2024-01-12T09:14:18.025Z
Date de création dans IRIS
2025-05-21T06:36:23Z
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