Key result
Genetic invalidation of Tenascin-C in knockout mice abrogated inflammation and monocyte/macrophage recruitment, leading to less ventricular remodeling and improved cardiac function after transverse aortic constriction compared with wild-type mice.
Population
12-week-old male mice (wild-type and TNC knockout)
Comparison
Transverse aortic constriction or administration… vs Wild-type mice
Design
Preclinical
Follow-up
1 week
Authors
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Tenascin-C ablation attenuates remodeling in murine pressure overload; hypothesis-generating for inhibition in human HF.
Tenascin-C promotes a pro-inflammatory microenvironment and macrophage migration in fibrotic hearts, suggesting its inhibition could be a therapeutic strategy for heart disease.
Abbadi et al. (2017) studied Pressure overload-induced cardiac dysfunction. Tenascin-C (TNC) genetic invalidation (knockout) vs. Wild-type mice was evaluated on Cardiac dysfunction, monocyte/macrophage accumulation, and ventricular remodeling. Genetic invalidation of Tenascin-C in knockout mice abrogated inflammation and monocyte/macrophage recruitment, leading to less ventricular remodeling and improved cardiac function after transverse aortic constriction compared with wild-type mice.
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