ArticleBritish journal of pharmacology2014
Inhibition of PKC-θ preserves cardiac function and reduces fibrosis in streptozotocin-induced diabetic cardiomyopathy.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Exercise Empowerment: A Multifaceted Anatomy in Managing Diabetic Myocardial Disorder.Journal of cardiovascular translational research · 2025Review
- Metabolic and Mitochondrial Dysregulations in Diabetic Cardiac Complications.International journal of molecular sciences · 2025Review
- The immunology of diabetic cardiomyopathy.Frontiers in endocrinology · 2025Review
- Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction.Journal of cardiovascular development and disease · 2023Article
- Molecular Mechanisms of Hawthorn Extracts in Multiple Organs Disorders in Underlying of Diabetes: A Review.International journal of endocrinology · 2022Review
- Profile of crosstalk between glucose and lipid metabolic disturbance and diabetic cardiomyopathy: Inflammation and oxidative stress.Frontiers in endocrinology · 2022Review
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Polydatin and polydatin-loaded chitosan nanoparticles attenuate diabetic cardiomyopathy in rats.Journal of molecular histology · 2021Article
- Subcellular microRNAs in diabetic cardiomyopathy.Annals of translational medicine · 2020Review
- Diabetic atherosclerosis: is there a role for the hypoxia-inducible factors?Bioscience reports · 2020Review
- Epigenetic Alterations Are Associated With Gastric Emptying Disturbances in Diabetes Mellitus.Clinical and translational gastroenterology · 2020Observational
- Advanced glycation end products facilitate the proliferation and reduce early apoptosis of cardiac microvascular endothelial cells via PKCβ signaling pathway: Insight from diabetic cardiomyopathy.Anatolian journal of cardiology · 2020Article
- Article
- Cardiac contractile dysfunction and protein kinase C-mediated myofilament phosphorylation in disease and aging.The Journal of general physiology · 2019Article
- PKC and PKN in heart disease.Journal of molecular and cellular cardiology · 2019Review
- Diabetic Cardiomyopathy: An Update of Mechanisms Contributing to This Clinical Entity.Circulation research · 2018Review
- Identification of Core Gene Biomarkers in Patients with Diabetic Cardiomyopathy.Disease markers · 2018Article
- The Role of Allograft Inflammatory Factor-1 in the Effects of Experimental Diabetes on B Cell Functions in the Heart.Frontiers in cardiovascular medicine · 2018Article
- Mechanisms of cardioprotection via modulation of the immune response.Current opinion in pharmacology · 2017Review
- Heat shock transcription factor 1 protects against pressure overload-induced cardiac fibrosis via Smad3.Journal of molecular medicine (Berlin, Germany) · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeT-cell infiltration, interstitial fibrosis and cardiac dysfunction have been observed in diabetic patients with cardiovascular diseases. PKC-θ is crucial for the activation of mature T-cells. We hypothesized that inhibition of PKC-θ might protect diabetic hearts through inhibition of T-cell stimulation and maintenance of tight junction integrity. EXPERIMENTAL APPROACH: A model of type 1 diabetes was induced by streptozotocin (STZ) (50 mg kg(-1) for 5 days) in male C57BL/6J wild-type (WT) mice and Rag1 knockout (KO) mice which lack mature lymphocytes. A cell-permeable selective PKC-θ peptide inhibitor (PI) was administered i.p. (0.2 mg kg(-1) ·day(-1) ) for 4 weeks (first phase) and 2 weeks (second phase). At the end of the 11th week, cardiac contractile force was measured in isolated perfused hearts. Cardiac morphology and fibrosis were determined. Phosphorylation of PKC-θ at Tyr(358) , infiltrated T-cells and tight junction protein ZO-1 within the hearts were detected, using immunohistochemcial techniques. KEY
resultsPI did not affect high blood glucose level in both WT and Rag1 KO diabetic mice. Diabetes induced cardiac fibrosis in WT mice but not in Rag1 KO mice. PI attenuated cardiac fibrosis and improved cardiac contractility of WT diabetic hearts. PI decreased expression of phosphorylated PKC-θ, reduced the infiltration of T-cells and increased ZO-1 expression within WT diabetic hearts. CONCLUSION AND IMPLICATIONS: Inhibition of PKC-θ improves cardiac function and reduces cardiac fibrosis in WT mice with streptozotocin-induced diabetes. Mature T-cells play a key role in pathophysiology of diabetic cardiomyopathy.
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