miRNA profiling shows shared signatures in pediatric asthma, obesity and their comorbidity - Summary - MDSpire

miRNA profiling shows shared signatures in pediatric asthma, obesity and their comorbidity

  • By

  • Harshita Shailesh

  • Mohamed Nadhir Djekidel

  • Safa Noor

  • Lena Hayati

  • Stefan Worgall

  • Souhaila Al Khodor

  • Ibrahim Janahi

  • May 13, 2026

  • 0 min

Share

Objective:

To identify microRNA profiles associated with asthma–obesity comorbidity in children, thereby enhancing understanding of the underlying molecular pathways that may inform treatment strategies.

Key Findings:
  • Five miRNAs (miR-423-3p, -92a-3p, -4536-5p, -197-3p, -891a-5p) were consistently upregulated in asthma and obesity cohorts, indicating a potential link to disease severity.
  • Two miRNAs (miR-144-3p, -641) were downregulated in asthma-only, obesity-only, and asthma-obesity comorbidity groups, suggesting a common regulatory mechanism.
  • miRNAs associated with OO-A were linked to IL-4, IL-13, and PIP3/AKT signaling pathways, indicating roles in inflammation and metabolism.
  • Altered miRNA expression correlated with increased neutrophil counts, elevated pro-inflammatory cytokines, and reduced lung function in OO-A, highlighting the clinical relevance of these findings.
Interpretation:

The identified miRNA profiles suggest potential biomarkers and therapeutic targets for managing asthma in pediatric patients with obesity, underscoring the need for further validation to confirm their clinical utility.

Limitations:
  • Cross-sectional design limits causal inferences, making it difficult to establish direct relationships.
  • Small sample size may affect the generalizability of findings, necessitating caution in interpretation.
  • Further longitudinal studies are needed to validate miRNA as biomarkers and to explore their role in disease progression.
Conclusion:

This study uncovers a common circulating miRNA profile linked to asthma–obesity comorbidity, which may inform future therapeutic strategies.

Original Source(s)

Related Content