Articular cartilage is an avascular tissue that has a limited capacity for self-repair. Cell-based cartilage repair procedures require that autologous articular chondrocytes are isolated from a small biopsy, expanded in vitro, and then either directly injected into the defect or used to engineer implantable grafts. Although medium- and long-term results regarding these procedures are satisfactory, still a certain percentage of autologous chondrocyte-based procedures lead to unsuccessful and unsatisfactory clinical outcomes. The acquisition of morphological alterations (i.e., loss of the chondrocyte phenotype and acquisition of senescing traits) by articular chondrocytes during their ex vivo culture is one of the main causes pampering the capacity of these cells to produce functional tissues.
New strategies/conditionings allowing to counteract these aberrant chondrocyte features and thus their regenerative capacity are then needed.
Here we aim to prepare a collection of manuscripts, Original Research, and Reviews, describing and explaining methodologies, strategies, and molecular mechanisms promoting or enhancing the chondrogenic potential of articular chondrocytes.
Areas to be covered in this Research Topic include, but are not limited to:
• Use of bioactive components (growth factors, morphogens, small molecule compounds) to enhance proliferation/chondrogenic capacity of chondrocytes
• Use of mechanical stimulation systems (ultrasound, Pulsed Electromagnetic Field Therapy, PEFP) to boost the chondrogenic potentiality of chondrocytes
• Genetic modification strategies (gene addition, gene correction, gene silencing, and gene editing
• New 3D culturing systems (scaffolds, biomaterials, devices)
• Preconditioning (hypoxic culture, cytokines/small molecules, physical factors) to improve chondrocyte performance in vitro or in vivo
• Strategies to counteract chondrocytes de-differentiation during their vitro culture (culture temperature, hypoxia, 3D culture, extracellular matrix, hydrogel, 3D bioprinting)
• Strategies to reduce cellular senescence in chondrocytes (senolytic drugs/agents, secretome, ECM, microRNAs)
Articular cartilage is an avascular tissue that has a limited capacity for self-repair. Cell-based cartilage repair procedures require that autologous articular chondrocytes are isolated from a small biopsy, expanded in vitro, and then either directly injected into the defect or used to engineer implantable grafts. Although medium- and long-term results regarding these procedures are satisfactory, still a certain percentage of autologous chondrocyte-based procedures lead to unsuccessful and unsatisfactory clinical outcomes. The acquisition of morphological alterations (i.e., loss of the chondrocyte phenotype and acquisition of senescing traits) by articular chondrocytes during their ex vivo culture is one of the main causes pampering the capacity of these cells to produce functional tissues.
New strategies/conditionings allowing to counteract these aberrant chondrocyte features and thus their regenerative capacity are then needed.
Here we aim to prepare a collection of manuscripts, Original Research, and Reviews, describing and explaining methodologies, strategies, and molecular mechanisms promoting or enhancing the chondrogenic potential of articular chondrocytes.
Areas to be covered in this Research Topic include, but are not limited to:
• Use of bioactive components (growth factors, morphogens, small molecule compounds) to enhance proliferation/chondrogenic capacity of chondrocytes
• Use of mechanical stimulation systems (ultrasound, Pulsed Electromagnetic Field Therapy, PEFP) to boost the chondrogenic potentiality of chondrocytes
• Genetic modification strategies (gene addition, gene correction, gene silencing, and gene editing
• New 3D culturing systems (scaffolds, biomaterials, devices)
• Preconditioning (hypoxic culture, cytokines/small molecules, physical factors) to improve chondrocyte performance in vitro or in vivo
• Strategies to counteract chondrocytes de-differentiation during their vitro culture (culture temperature, hypoxia, 3D culture, extracellular matrix, hydrogel, 3D bioprinting)
• Strategies to reduce cellular senescence in chondrocytes (senolytic drugs/agents, secretome, ECM, microRNAs)
