Osteoarthritis is a degenerative joint disease and a major disease context for studying growth factor mechanisms, with bibliometric work mapping research trends and knowledge structures from 2005 to 2024. It is strongly linked to the tgf beta superfamily, which was identified as the most frequently studied growth factor group in osteoarthritis research and is implicated in cartilage repair and inflammatory modulation. Other associated factors include igf, tied to chondrogenesis, ngf, tied to neural regulation, and vegf, tied to angiogenesis. Recent work also suggests a therapeutic mechanism for artificial mitochondria, which ameliorates osteoarthritis by restoring cellular energy metabolism homeostasis in a murine knee model via intra-articular CAM injections. Overall, the literature frames osteoarthritis as both a cartilage-degenerative and inflammation-associated condition with active interest in growth factor signaling and regenerative interventions.
Growth factor mechanisms
- A 2026 bibliometric study (PMID:41890882) mapped research trends and knowledge structures on growth factors in osteoarthritis across 2005–2024, highlighting the field’s evolution.
- The tgf beta superfamily was reported as the most frequently studied growth factor group in osteoarthritis research and was linked to cartilage repair and inflammatory modulation. (PMID:41890882)
- igf was described as strongly associated with chondrogenesis in osteoarthritis. (PMID:41890882)
- ngf was described as strongly associated with neural regulation in osteoarthritis. (PMID:41890882)
- vegf was described as strongly associated with angiogenesis in osteoarthritis. (PMID:41890882)
Therapeutic delivery and regeneration
- A 2026 Bioactive Materials study (PMID:41816316) reported that artificial mitochondria ameliorates osteoarthritis by restoring cellular energy metabolism homeostasis.
- In that study, treatment was evaluated in a murine knee model using intra-articular CAM injections. (PMID:41816316)
- The findings support a regenerative/metabolic intervention strategy for degenerative joint disease rather than only symptom control. (PMID:41816316)