ArticleJournal of molecular medicine (Berlin, Germany)2014
FP-receptor gene silencing ameliorates myocardial fibrosis and protects from diabetic cardiomyopathy.
Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- New Locus for Skin Intrinsic Fluorescence in Type 1 Diabetes Also Associated With Blood and Skin Glycated Proteins.Diabetes · 2016Pooled it
- Calcium dysregulation in diabetic cardiomyopathy & heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2026Review
- Burns: The "Fuse" That Ignites Organ Crisis - A Narrative Review of Mechanisms and Crosstalk in Post-Burn MODS.Journal of inflammation research · 2026Review
- Prostaglandin DCells · 2025Article
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Human umbilical cord-derived mesenchymal stromal cells improve myocardial fibrosis and restore miRNA-133a expression in diabetic cardiomyopathy.Stem cell research & therapy · 2024Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- The Link between Prostanoids and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Comparison of the Drug-Induced Efficacies between Omidenepag Isopropyl, an EP2 Agonist and PGF2α toward TGF-β2-Modulated Human Trabecular Meshwork (HTM) Cells.Journal of clinical medicine · 2022Article
- Enzymes Present in Neutrophil Extracellular Traps May Stimulate the Fibrogenic PGFAnimals : an open access journal from MDPI · 2021Article
- Screening of the Drug-Induced Effects of Prostaglandin EP2 and FP Agonists on 3D Cultures of Dexamethasone-Treated Human Trabecular Meshwork Cells.Biomedicines · 2021Article
- The Roles of Various Prostaglandins in Fibrosis: A Review.Biomolecules · 2021Review
- Aminoguanidine reduces diabetes-associated cardiac fibrosis.Experimental and therapeutic medicine · 2019Article
- Deletion of RasGRF1 Attenuated Interstitial Fibrosis in Streptozotocin-Induced Diabetic Cardiomyopathy in Mice through Affecting Inflammation and Oxidative Stress.International journal of molecular sciences · 2018Article
- Resveratrol attenuates high glucose-induced cardiomyocytes injury via interfering ROS-MAPK-NF-κB signaling pathway.International journal of clinical and experimental pathology · 2018Article
- Salusin-β contributes to oxidative stress and inflammation in diabetic cardiomyopathy.Cell death & disease · 2017Article
- Quantitative assessment of myocardial fibrosis in an age-related rat model by ex vivo late gadolinium enhancement magnetic resonance imaging with histopathological correlation.Computers in biology and medicine · 2015Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledProstaglandin F2(α)-F-prostanoid (PGF2(α)-FP) receptor is closely related to insulin resistance, which plays a causal role in the pathogenesis of diabetic cardiomyopathy (DCM). We sought to reveal whether PGF2(α)-FP receptor plays an important part in modulating DCM and the mechanisms involved. We established the type 2 diabetes rat model by high-fat diet and low-dose streptozotocin (STZ) and then evaluated its characteristics by metabolite tests, Western blot analysis for FP-receptor expression, histopathologic analyses of cardiomyocyte density and fibrosis area. Next, we used gene silencing to investigate the role of FP receptor in the pathophysiologic features of DCM. Our study showed elevated cholesterol, triglyceride, glucose, and insulin levels, severe insulin resistance, and FP-receptor overexpression in diabetic rats. The collagen volume fraction (CVF) and perivascular collagen area/luminal area (PVCA/LA) were higher in the diabetic group than the control group (CVF% 10.99 ± 0.99 vs 1.59 ± 0.18, P < 0.05; PVCA/LA% 17.07 ± 2.61 vs 2.86 ± 0.69, P < 0.05). We found that the silencing of FP receptor decreased cholesterol, triglyceride, glucose, and insulin levels and ameliorated insulin resistance. The CVF and PVCF/LA were significantly downregulated in FP-receptor short hairpin RNA (shRNA) treatment group (FP-receptor shRNA group vs vehicle group: CVF% 5.59 ± 0.92 vs 10.97 ± 1.33, P < 0.05, PVCA/LA% 4.74 ± 1.57 vs 14.79 ± 2.22, P < 0.05; FP-receptor shRNA + PGF2(α) group vs vehicle group : CVF% 5.19 ± 0.79 vs 10.97 ± 1.33, P < 0.05, PVCA/LA% 5.96 ± 1.15 vs 14.79 ± 2.22, P < 0.05, respectively). Furthermore, with FP-receptor gene silencing, the activated protein kinase C (PKC) and Rho kinase were significantly decreased, and the blunted phosphorylation of Akt was restored. FP-receptor gene silencing may exert a protective effect on DCM by improving myocardial fibrosis, suggesting a new therapeutic approach for human DCM. KEY MESSAGES: FP-receptor gene silencing improves glucose tolerance and insulin resistance in type 2 diabetes (T2D). FP-receptor gene silencing modulates the activities of PKC/Rho and Akt signaling pathways in T2D. FP-receptor gene silencing decreases collagen expression and ameliorates myocardial fibrosis in T2D. FP-receptor gene silencing protects from diabetic cardiomyopathy in T2D.
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