Nanomedicine-Driven Approaches for Kartogenin Delivery: Advancing Chondrogenic Differentiation and Cartilage Regeneration in Tissue Engineering
Bhuyan S., Swain S., Misra RDK., Rautray TR.
Narrative Review on Osteoarthritis, Cartilage Damage, Tendon Injury, published in Int J Nanomedicine (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Int J Nanomedicine (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40535835
- PMCID
- PMC12174920
- DOI
- 10.2147/ijn.s525580
Abstract (original English)
Articular cartilage degradation and osteocartilage defects are the most prevalent concerns that vary from localized to more systemic forms of cartilage disease. However, regulating chondrogenic differentiation within the joints remains a significant challenge. Kartogenin, a small heterocyclic compound, has recently garnered considerable attention as a potential therapeutic agent, owing to both chondrogenic and chondroprotective properties for intra-articular therapy. Initially, it was created for osteoarthritis; it has also been used to address various diseased conditions, such as the regeneration of disc and bone-tendon junctions. On top of that, it preserves the equilibrium between cartilage catabolism and anabolism, while also mitigating inflammation and alleviating pain by preventing damage induced by cytokines. To modulate tissue function and cellular behaviour, it is crucial to have sustained release of ketogenic through an appropriate delivery system. A multitude of biomaterial-based carriers have been developed for the prolonged release of kartogenin. Moreover, many biological mechanisms of action of kartogenin have been identified. The most critical molecular mechanism among them is the dissociation of filamin A from core-binding factor (CBF)-β induced by kartogenin. Filamin A subsequently translocates to the nucleus, where it engages with RUNX-1 to transcribe genes im
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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