Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2025 Mar 26:13:1522303.
doi: 10.3389/fbioe.2025.1522303. eCollection 2025.

Non-coding RNA in cartilage regeneration: regulatory mechanism and therapeutic strategies

Affiliations
Review

Non-coding RNA in cartilage regeneration: regulatory mechanism and therapeutic strategies

Mengnan Wen et al. Front Bioeng Biotechnol. .

Abstract

The pathogenesis of cartilage injury and degeneration is exceptionally complex. In addition to being associated with osteoarthritis and trauma, factors such as age, gender, obesity, inflammation, and apoptosis of chondrocytes are also considered significant influencing factors. Due to the lack of direct blood supply, lymphatic circulation, and neural innervation, coupled with low metabolic activity, the self-repair capability of cartilage after injury is extremely limited, making its treatment quite challenging. Recent research indicated that ncRNA, a class of RNA transcribed from the genome that does not encode proteins, played a crucial regulatory role in various disease processes. Particularly noteworthy is its positive regulatory role in cartilage regeneration, achieved through the modulation of the inflammatory microenvironment, promotion of chondrocyte proliferation, inhibition of chondrocyte degradation, and facilitation of the recruitment and differentiation of bone marrow mesenchymal stem cells into chondrocytes. In the earlier phase, we conducted a review and outlook on therapeutic strategies for the regeneration of articular cartilage injuries. This article specifically focuses on summarizing the regulatory roles and research advancements of ncRNA in cartilage regeneration, as well as its contributions to the clinical application of gene therapy for cartilage defects.

Keywords: OA; cartilage regeneration; gene therapy; non-coding RNA; tissue engineering and regenerative medicine.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Gene transfer methods.
FIGURE 2
FIGURE 2
The location of non-coding RNA.
FIGURE 3
FIGURE 3
The process of cartilage development.
FIGURE 4
FIGURE 4
The mechanism of action of circRNA3503 in OA.
FIGURE 5
FIGURE 5
The VEGFα siRNA encapsulated in LNPs promotes cartilage formation by inhibiting angiogenesis.

Similar articles

References

    1. Barter M. J., Gomez R., Hyatt S., Cheung K., Skelton A., Xu Y., et al. (2017). Long noncoding RNA ROCR contributes to SOX9 expression and chondrogenic differentiation of human mesenchymal stem cells. Dev. Dev., 152504. 10.1242/dev.152504 - DOI - PMC - PubMed
    1. Breda L., Papp T. E., Triebwasser M. P., Yadegari A., Fedorky M. T., Tanaka N., et al. (2023). In vivo hematopoietic stem cell modification by mRNA delivery. Science 381, 436–443. 10.1126/science.ade6967 - DOI - PMC - PubMed
    1. Cao Y., Tang S., Nie X., Zhou Z., Ruan G., Han W., et al. (2021). Decreased miR-214–3p activates NF-κB pathway and aggravates osteoarthritis progression. EBioMedicine 65, 103283. 10.1016/j.ebiom.2021.103283 - DOI - PMC - PubMed
    1. Caramés B., Hasegawa A., Taniguchi N., Miyaki S., Blanco F. J., Lotz M. (2012). Autophagy activation by rapamycin reduces severity of experimental osteoarthritis. Ann. Rheum. Dis. 71, 575–581. 10.1136/annrheumdis-2011-200557 - DOI - PMC - PubMed
    1. Carpio L. R., Westendorf J. J. (2016). Histone deacetylases in cartilage homeostasis and osteoarthritis. Curr. Rheumatol. Rep. 18, 52. 10.1007/s11926-016-0602-z - DOI - PubMed

LinkOut - more resources