---
title: "Muscle miRNAs as cell-intrinsic epigenetic regulators in type 2 diabetes"
id: "pubmed-42680724"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42680724"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42680724/"
doi: "10.1038/s41392-026-02846-7"
published_at: "2026-09-02T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Muscle miRNAs as cell-intrinsic epigenetic regulators in type 2 diabetes
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42680724
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42680724/)
- **DOI:** [10.1038/s41392-026-02846-7](https://doi.org/10.1038%2Fs41392-026-02846-7)
- **Published At:** 2026-09-02T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study used a disease-in-a-dish model: induced pluripotent stem cells (iPSCs) from people with type 2 diabetes (T2D) and controls were differentiated into myoblasts (iMyos) to test cell-intrinsic effects on microRNA expression and secretion. - **miRNAs** were altered in T2D iMyos at both the cellular level and in secretion via **small extracellular vesicles (sEVs)/exosomes**, indicating cell-autonomous dysregulation independent of the in vivo milieu. - Integration of miRNA target predictions with transcriptomic and proteomic data showed that altered miRNAs in T2D iMyos were associated with coordinated changes in predicted targets, with a greater measurable impact on **protein** than on mRNA levels. - Experimental overexpression of selected miRNAs in control iMyos validated the stronger effect on protein expression compared with mRNA. - Upregulated miRNAs in T2D iMyos targeted pathways related to **aerobic respiration**, membrane trafficking, and RNA metabolism; secreted miRNAs were enriched for targets in metabolic pathways including **insulin signaling** and **mitochondrial metabolism**. - sEVs from control iMyos increased glucose uptake and mitochondrial function in recipient human white adipocytes, whereas sEVs from T2D iMyos failed to induce these effects, supporting functional consequences of altered miRNA secretion. - The findings support a model in which muscle in T2D displays cell-intrinsic changes in miRNA expression and selective secretion that act as **epigenetic regulators** of protein expression locally and potentially in distal tissues. - Conflict of interest: authors declared no competing interests. Details such as donor numbers, specific miRNA identities, and exact quantitative results were not reported in the provided abstract.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. * 2 Genetics and Epidemiology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. * 3 Metabolism Unit and Division of Endocrinology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. * 4 Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. c.ronald.kahn@joslin.harvard.edu. * PMID: **42680724** * DOI: [ 10.1038/s41392-026-02846-7 ](https://doi.org/10.1038/s41392-026-02846-7) Item in Clipboard # miRNAs as cell-intrinsic epigenetic regulators in muscle in type 2 diabetes Allah Nawaz et al. Signal Transduct Target Ther. 2026. Show details Display options Display options Format Abstract PubMed PMID Signal Transduct Target Ther Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Signal+Transduct+Target+Ther%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Signal+Transduct+Target+Ther%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) . 2026 Sep 2;11(1):359. doi: 10.1038/s41392-026-02846-7. ### Authors [Allah Nawaz](https://pubmed.ncbi.nlm.nih.gov/?term=Nawaz+A&cauthor_id=42680724)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-1 "Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA."), [Marsel Lino](https://pubmed.ncbi.nlm.nih.gov/?term=Lino+M&cauthor_id=42680724)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-1 "Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA."), [Nida Haider](https://pubmed.ncbi.nlm.nih.gov/?term=Haider+N&cauthor_id=42680724)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-1 "Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA."), [Antonio S Gomes](https://pubmed.ncbi.nlm.nih.gov/?term=Gomes+AS&cauthor_id=42680724)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-1 "Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA."), [Anindya Ghosh](https://pubmed.ncbi.nlm.nih.gov/?term=Ghosh+A&cauthor_id=42680724)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-1 "Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA."), [Eiichiro Satake](https://pubmed.ncbi.nlm.nih.gov/?term=Satake+E&cauthor_id=42680724)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-2 "Genetics and Epidemiology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA."), [Arijeet K Gattu](https://pubmed.ncbi.nlm.nih.gov/?term=Gattu+AK&cauthor_id=42680724)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-1 "Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-3 "Metabolism Unit and Division of Endocrinology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA."), [C Ronald Kahn](https://pubmed.ncbi.nlm.nih.gov/?term=Kahn+CR&cauthor_id=42680724)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42680724/#short-view-affiliation-4 "Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. c.ronald.kahn@joslin.harvard.edu.") ### Affiliations * 1 Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. * 2 Genetics and Epidemiology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. * 3 Metabolism Unit and Division of Endocrinology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. * 4 Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. c.ronald.kahn@joslin.harvard.edu. * PMID: **42680724** * DOI: [ 10.1038/s41392-026-02846-7 ](https://doi.org/10.1038/s41392-026-02846-7) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract miRNAs are important metabolic regulators and are altered at both the cellular and secreted levels in diseases, including type 2 diabetes (T2D). However, to what extent these alterations are in response to factors in the in vivo milieu or are cell-intrinsic remains unclear. Here we used a disease-in-a-dish model in which iPSCs from T2D patients and controls were differentiated into myoblasts (iMyos), and their cellular and secreted miRNAs were profiled. We found that iMyos from T2D donors exhibit cell-intrinsic alterations in miRNA expression and secretion in small extracellular vesicles (sEVs)/exosomes. Integrating miRNA-predicted targets with transcriptomic and proteomic data revealed that miRNAs altered in T2D iMyos were associated with coordinated changes in their predicted targets, but with a much greater impact on protein than on mRNA levels. This effect was validated by miRNA overexpression in control iMyos. The upregulated miRNAs targeted pathways related to aerobic respiration, membrane trafficking, and RNA metabolism. Even more marked changes were observed in sEV-associated miRNAs secreted by T2D iMyos, indicative of T2D-associated effects on miRNA sorting and release. Target genes of secreted miRNAs altered in T2D iMyos were enriched in metabolic pathways including insulin signaling and mitochondrial metabolism. Consistent with this, sEVs derived from control iMyos increased glucose uptake and mitochondrial function in recipient human white adipocytes, whereas sEVs from T2D iMyos did not. Thus, in T2D, muscle exhibits cell-intrinsic alterations in expression and secretion of miRNAs, which function as epigenetic regulators of protein expression locally, as well as potentially in distal tissues. © 2026. The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Competing interests: The authors declare no competing interests. ## References 1. 1. DeFronzo, R. A. & Tripathy, D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care 32, S157–S163 (2009). - [PubMed](https://pubmed.ncbi.nlm.nih.gov/19875544/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/2811436/) - [DOI](https://doi.org/10.2337/dc09-s302) 2. 1. Petersen, M. C. & Shulman, G. I. Mechanisms of insulin action and insulin resistance. Physiol. Rev. 98, 2133–2223 (2018). - [PubMed](https://pubmed.ncbi.nlm.nih.gov/30067154/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/6170977/) - [DOI](https://doi.org/10.1152/physrev.00063.2017) 3. 1. Petersen, K. F. & Shulman, G. I. Pathogenesis of skeletal muscle insulin resistance in type 2 diabetes mellitus. Am. J. Cardiol. 90, 11g–18g (2002). - [PubMed](https://pubmed.ncbi.nlm.nih.gov/12231074/) - [DOI](https://doi.org/10.1016/s0002-9149\(02\)02554-7) 4. 1. Martin, B. C. et al. Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet 340, 925–929 (1992). - [PubMed](https://pubmed.ncbi.nlm.nih.gov/1357346/) - [DOI](https://doi.org/10.1016/0140-6736\(92\)92814-v) 5. 1. Batista, T. M. et al. A cell-autonomous signature of dysregulated protein phosphorylation underlies muscle insulin resistance in type 2 diabetes. Cell Metab. 32, 844–859.e845 (2020). - [PubMed](https://pubmed.ncbi.nlm.nih.gov/32888406/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/7875546/) - [DOI](https://doi.org/10.1016/j.cmet.2020.08.007) Show all 90 references ## MeSH terms * Diabetes Mellitus, Type 2* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Type+2%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Type+2) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Diabetes Mellitus, Type 2* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Type+2%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Type+2) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Diabetes Mellitus, Type 2* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Type+2%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Type+2) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Epigenesis, Genetic* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Epigenesis%2C+Genetic%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Epigenesis%2C+Genetic) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Exosomes / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Exosomes%2Fgenetics%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Exosomes) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Humans Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Humans%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Humans) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * MicroRNAs* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22MicroRNAs%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=MicroRNAs) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Muscle, Skeletal / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Muscle%2C+Skeletal%2Fmetabolism%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Muscle%2C+Skeletal) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Muscle, Skeletal / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Muscle%2C+Skeletal%2Fpathology%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Muscle%2C+Skeletal) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Myoblasts / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Myoblasts%2Fmetabolism%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Myoblasts) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42680724/) * Myoblasts / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Myoblasts%2Fpathology%22%5BMeSH%5D&sort=d
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