ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2023
Replacement substance P reduces cardiac fibrosis in monkeys with type 2 diabetes.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Trial
- Neurokinin-1 receptor activation protects against cardiac fibrosis, inflammation and diastolic dysfunction in type 2 diabetic mice.British journal of pharmacology · 2026Article
- The first oral relaxin receptor RXFP1 agonist for heart failure treatment: Translational studies from non-human primates to humans.Molecular therapy. Advances · 2026Article
- T-Cell Signaling Pathways, Including Exhaustion, Predominate in Unhealthy Visceral and Subcutaneous Adipose Tissues.Obesity (Silver Spring, Md.) · 2026Article
- Cardiac fibrosis: from mechanisms and models to medicines.Trends in pharmacological sciences · 2025Review
- Cellular metabolism of substance P produces neurokinin-1 receptor peptide agonists with diminished cyclic AMP signaling.American journal of physiology. Cell physiology · 2024Article
- Potentiation of Collagen Deposition by the Combination of Substance P with Transforming Growth Factor Beta in Rat Skin Fibroblasts.International journal of molecular sciences · 2024Article
- Salvianolic acid B ameliorates myocardial fibrosis in diabetic cardiomyopathy by deubiquitinating Smad7.Chinese medicine · 2023Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundType 2 diabetes mellitus (T2DM)-associated cardiac fibrosis contributes to heart failure. We previously showed that diabetic mice with cardiomyopathy, including cardiac fibrosis, exhibit low levels of the neuropeptide substance P; exogenous replacement of substance P reversed cardiac fibrosis, independent of body weight, blood glucose and blood pressure. We sought to elucidate the effectiveness and safety of replacement substance P to ameliorate or reverse cardiac fibrosis in type 2 diabetic monkeys.
methodsFour female T2DM African Green monkeys receive substance P (0.5 mg/Kg/day S.Q. injection) for 8 weeks. We obtained cardiac magnetic resonance imaging and blood samples to assess left ventricular function and fibrosis by T1 map-derived extracellular volume as well as circulating procollagen type I C-terminal propeptide. Hematological parameters for toxicities were also assessed in these monkeys and compared with three female T2DM monkeys receiving saline S.Q. as a safety comparison group.
resultsDiabetic monkeys receiving replacement substance P exhibited a ∼20% decrease in extracellular volume (p = 0.01), concomitant with ∼25% decrease procollagen type I C-terminal propeptide levels (p = 0.008). Left ventricular ejection fraction was unchanged with substance P (p = 0.42); however, circumferential strain was improved (p < 0.01). Complete blood counts, glycosylated hemoglobin A1c, lipids, liver and pancreatic enzymes, and inflammation markers were unchanged (p > 0.05).
conclusionsReplacement substance P reversed cardiac fibrosis in a large preclinical model of type 2 diabetes, independent of glycemic control. No hematological or organ-related toxicity was associated with replacement substance P. These results strongly support a potential application for replacement substance P as safe therapy for diabetic cardiac fibrosis.
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