MicroRNAs in fetal alcohol spectrum disorders: A systematic review of prenatal exposure and molecular targets.

BACKGROUND

Fetal alcohol spectrum disorder (FASD), caused by prenatal ethanol exposure, encompasses developmental abnormalities such as craniofacial dysmorphism, sensory and motor impairments, and neurocognitive deficits. MicroRNAs have been proposed as key regulators in FASD pathophysiology, yet the specific molecular pathways they influence remain unclear.

METHODS

To better understand the role of microRNAs in the progression of FASD, we have systematically reviewed the effects of prenatal exposure to alcohol on microRNAs. The search was performed through PubMed MEDLINE, web of science, Scopus, and Google Scholar for all articles between 2006 and 2025.

RESULTS

The range of ethanol concentrations as well as exposure pattern which applied in the animal models were widely distributed. Totally, 241 differentially expressed microRNAs were identified from 36 experimentally published reports. Emerging data have implicated that special miRNAs are involved in apoptosis (e.g., miR-335, miR-21, miR-9, miR-29a), axon guidance (e.g., miR-17-5p, miR-10b-3p, let-7a-3p, let-7g-3p, let-7i-3p), cell migration/proliferation (e.g., miR760, miR-98-5p, miR-378a-3p), and up- or downregulations of proteins associated with FASD's abnormalities.

CONCLUSIONS

Despite substantial heterogeneity in experimental designs, including differences in model systems, species, dosing regimens, and exposure durations, several microRNAs (miR‑9, miR‑335, miR‑15b, miR‑34a, let‑7i, miR‑200a, and miR‑326) consistently emerge as key regulators implicated in the pathophysiology of fetal alcohol spectrum disorders.