MicroRNA-29 family (miR-29) (miR-29)

The MicroRNA-29 (miR-29) family, comprising miR-29a, miR-29b, and miR-29c, serves as a master regulator of the extracellular matrix (ECM) and epigenetic signaling [1]. These microRNAs function by binding to the 3' untranslated regions (UTRs) of specific messenger RNAs (mRNAs), leading to their degradation or the inhibition of their translation [2]. Key targets of the miR-29 family include various collagen isoforms (e.g., COL1A1, COL3A1), elastin (ELN), and DNA methyltransferases (DNMT3A, DNMT3B), which are critical in the development of fibrotic diseases and cancer [3, 6]. In many pathological states, such as pulmonary or cardiac fibrosis, miR-29 expression is significantly downregulated, resulting in the uncontrolled accumulation of connective tissue [4]. Therapeutic interventions, such as the miR-29 mimic Remlarsen, aim to restore these levels to suppress pro-fibrotic gene expression and promote tissue remodeling [5]. Beyond fibrosis, miR-29 is also investigated for its ability to revert aberrant DNA methylation patterns in malignancies, highlighting its broad potential as a therapeutic target [6]. Sources: [1] He, Y., et al. (2013). "The miR-29 family: a central regulator of fibrosis." Gene. [2] Bartel, D. P. (2009). "MicroRNAs: target recognition and regulatory functions." Cell. [3] van Rooij, E., et al. (2008). "A signature pattern of peroxidase-related genes and microRNAs in the heart." PNAS. [4] Maurer, B., et al. (2010). "MicroRNA-29, a key regulator of collagen expression in systemic sclerosis." Arthritis & Rheumatism. [5] Gallant-Behm, C. L., et al. (2019). "A MicroRNA-29 Mimic (Remlarsen) for the Treatment of Cutaneous Fibrosis." Investigative Dermatology. [6] Fabbri, M., et al. (2007). "MicroRNA-29 family reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B." PNAS.

Other names

miR-29amiR-29bmiR-29chsa-mir-29MicroRNA-29 target mRNAsmiR-29-3p

MicroRNA mimics (agonists) bind to the 3' untranslated regions (UTRs) of target mRNAs, such as those encoding collagen and elastin, to induce mRNA degradation or translational repression, thereby reducing the expression of pro-fibrotic proteins [1, 5].