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Related Experiment Video

Updated: Jun 14, 2025

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
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Diabetes Advances Cardiomyocyte Senescence Through Interfering Rnd3 Expression and Function.

Linxu Wu1,2, Xinglin Zhu1, Shanshan Pan1

  • 1Key Laboratory of Tropical Translational Medicine of Ministry of Education & Hainan Provincial Key Laboratory for Tropical Cardiovascular Diseases Research, School of Public Health, Hainan Medical University, Haikou, China.

Aging Cell
|March 3, 2025
PubMed
Summary

Diabetes accelerates heart aging by reducing Rnd3, a protein crucial for preventing cell senescence. Restoring Rnd3 levels may offer a new treatment for diabetic cardiomyopathy (DCM).

Keywords:
Rnd3STAT3cardiomyocytecellular senescencediabetic cardiomyopathymiR‐103a‐3p

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Area of Science:

  • Cardiovascular Biology
  • Cellular Senescence
  • Diabetic Complications

Background:

  • Rnd3, a Rho-GTPase, is linked to cardiovascular diseases, but its role in diabetes-induced cardiomyocyte senescence is unclear.
  • Diabetic cardiomyopathy (DCM) is a significant complication of diabetes, characterized by impaired cardiac function and cellular changes.
  • Aging increases susceptibility to cardiac dysfunction, with older rats exhibiting impaired cardiac function and elevated senescence markers.

Purpose of the Study:

  • To investigate the role of Rnd3 in cardiomyocyte senescence and diabetic cardiomyopathy (DCM).
  • To elucidate the molecular mechanisms underlying Rnd3 regulation and its impact on cardiac function in diabetes.
  • To identify potential therapeutic targets for mitigating diabetes-induced heart aging and dysfunction.

Main Methods:

  • Assessed Rnd3 expression in diabetic patients and Sprague Dawley (SD) rats of different ages.
  • Induced cardiomyocyte senescence using high glucose (HG) conditions in vitro and in vivo.
  • Utilized microRNA sequencing, AAV9 vectors for gene manipulation, and STAT3 inhibitors to explore signaling pathways.

Main Results:

  • Rnd3 expression was reduced in diabetic patients and cardiomyocytes under HG conditions, exacerbating senescence.
  • miR-103a-3p was identified as a key regulator, suppressing Rnd3 and promoting senescence; its inhibition alleviated HG-induced effects.
  • Rnd3 deficiency worsened HG-induced STAT3 activation; Rnd3 interacted with p-STAT3, promoting its degradation and reducing senescence.

Conclusions:

  • Diabetes induces cardiomyocyte senescence and cardiac dysfunction through the miR-103a-3p/Rnd3/STAT3 signaling pathway.
  • Therapeutic strategies targeting this pathway, such as restoring Rnd3 or inhibiting miR-103a-3p, show promise for DCM.
  • Rnd3 plays a protective role against diabetes-induced cardiac aging by regulating STAT3 activity.