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This study aims to clarify the role of Tenascin-C in the development of diabetic cardiomyopathy (DCM).

February 22, 2026Open Access

Tenascin-C drives cardiovascular dysfunction in a mouse model of diabetic cardiomyopathy

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This study aims to clarify the role of Tenascin-C in the development of diabetic cardiomyopathy (DCM).
Induced diabetes in wild-type and TNC knockout mice using streptozotocin.
Evaluated cardiac and aortic function at 18 weeks with echocardiography and myography.
Conducted biochemical, histological, and molecular analyses of myocardial and plasma samples.
Investigated the effects of diabetes on TNC expression using cardiomyocytes and cardiac fibroblasts.
Performed RNA sequencing for transcriptomic analysis of cardiac tissue.
TNC knockout diabetic mice exhibited preserved cardiac function and reduced fibrosis compared to wild-type.
TNC-KO mice showed less myocardial stiffness under diabetic conditions.
High glucose significantly increased TNC expression in cardiomyocytes and fibroblasts.
Recombinant TNC caused inflammation and oxidative stress in cardiomyocytes.
Elevated plasma TNC levels were found in heart failure patients, independent of diabetes.

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Experimental study reveals TNC's critical role in cardiac dysfunction in diabetic mice, suggesting new treatment strategies.

Arnold et al. (2025) studied this question.

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