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MicroRNA-29 (miR-29) is a family of small non-coding RNAs, comprising miR-29a, miR-29b, and miR-29c, that acts as a master regulator of the extracellular matrix (ECM) [1]. It functions by binding to the 3' untranslated regions (UTRs) of a broad set of mRNAs encoding structural proteins such as collagen (e.g., COL1A1, COL3A1), elastin (ELN), and fibrillin (FBN1), as well as enzymes involved in ECM cross-linking [2]. In various fibrotic diseases, including pulmonary, cardiac, and hepatic fibrosis, miR-29 expression is typically downregulated, leading to the pathological overproduction of ECM components [3]. Therapeutic strategies focus on using miR-29 mimics, such as Remlarsen, to restore miR-29 activity and suppress the expression of these pro-fibrotic targets [4]. Beyond fibrosis, miR-29 also plays significant roles in cell proliferation and apoptosis, often acting as a tumor suppressor in several types of cancer [1].
MicroRNA mimicry leading to the sequence-specific degradation and translational inhibition of target mRNAs involved in extracellular matrix production.
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