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The role of miRNAs in polycystic ovary syndrome with insulin resistance

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Journal of Assisted Reproduction and Genetics Aims and scope Submit manuscript

Abstract

Purpose

This review aims to summarize the key findings of several miRNAs and their roles in polycystic ovary syndrome with insulin resistance, characterize the disease pathogenesis, and establish a new theoretical basis for diagnosing, treating, and preventing polycystic ovary syndrome.

Methods

Relevant scientific literature was covered from 1992 to 2020 by searching the PubMed database with search terms: insulin/insulin resistance, polycystic ovary syndrome, microRNAs, and metabolic diseases. References of relevant studies were cross-checked.

Results

The related miRNAs (including differentially expressed miRNAs) and their roles in pathogenesis, and possible therapeutic targets and pathways, are discussed, highlighting controversies and offering thoughts for future directions.

Conclusion

We found abundant evidence on the role of differentially expressed miRNAs with its related phenotypes in PCOS. Considering the essential role of insulin resistance in the pathogenesis of PCOS, the alterations of associated miRNAs need more research attention. We speculate that race/ethnicity or PCOS phenotype and differences in methodological differences might lead to inconsistencies in research findings; thus, several miRNA profiles need to be investigated further to qualify for the potential therapeutic targets for PCOS-IR.

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This work was supported by the National Natural Science Foundation of China (81571407).

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Yingliu Luo: Writing-original draft preparation and editing

Chenchen Cui: Writing-reviewing and editing

Xiao Han: Writing-reviewing, editing, and supervision

Qian Wang: Supervision

Cuilian Zhang: Supervision, project administration, and funding acquisition

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Correspondence to Cuilian Zhang.

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Luo, Y., Cui, C., Han, X. et al. The role of miRNAs in polycystic ovary syndrome with insulin resistance. J Assist Reprod Genet 38, 289–304 (2021). https://doi.org/10.1007/s10815-020-02019-7

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