ArticleBritish journal of pharmacology2026
Neurokinin-1 receptor activation protects against cardiac fibrosis, inflammation and diastolic dysfunction in type 2 diabetic mice.
Article in British journal of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
background and purposeThe pathogenesis of type 2 diabetes mellitus (T2DM)-induced cardiomyopathy involves cardiac fibrosis that leads to diastolic dysfunction. We established that replacement of lost substance P (SP) that occurs in T2DM reduces cardiac fibrosis and decreases inflammation in T2DM mice and non-human primates. This study aimed to identify the specific anti-fibrotic SP receptor. EXPERIMENTAL APPROACH: Age-matched male wild type (WT) and Lepr KEY
resultsNK-1R activation decreased cardiac fibrosis, improved diastolic function, decreased mast cell numbers and promoted an anti-inflammatory macrophage phenotype in Lepr CONCLUSION AND IMPLICATIONS: The NK-1R is the anti-fibrotic SP receptor and improves diastolic function in the diabetic heart. This likely involves direct effects on cardiac fibroblasts and macrophages. This study provides a potential target for treatment of diabetic cardiomyopathy.
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