Restoration of Angiogenesis by Enalapril in Diabetic Hindlimb Ischemc Rats

Fallahzadeh, Ali Reza; Khazaei, Majid; Sharifi, Mohammad Reza

doi:10.5507/bp.2011.026

Cited by 4 publications

(4 citation statements)

References 30 publications

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“…Food and water intake and body weight were also monitored. The dosage of Enalapril was selected based on reported animal studies 89 , 90 15 mg/kg Enalapril and 5 mg/kg hydralazine 91 were administered daily by intraperitoneal injection for three weeks, starting on the second day after UUO injury. Mice were monitored closely for 3 weeks after left ureter ligation.…”

Section: Methodsmentioning

confidence: 99%

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Ham

Jin

Lei

et al. 2018

Sci Rep

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Cardiovascular disease constitutes the leading cause of mortality in patients with chronic kidney disease (CKD) and end-stage renal disease. Despite increasing recognition of a close interplay between kidney dysfunction and cardiovascular disease, termed cardiorenal syndrome (CRS), the underlying mechanisms of CRS remain poorly understood. Here we report the development of pathological cardiac hypertrophy and fibrosis in early stage non-uremic CKD. Moderate kidney failure was induced three weeks after unilateral urinary obstruction (UUO) in mice. We observed pathological cardiac hypertrophy and increased fibrosis in UUO-induced CKD (UUO/CKD) animals. Further analysis indicated that this cardiac fibrosis was associated with increased expression of transforming growth factor β (TGF-β) along with significant upregulation of Smad 2/3 signaling in the heart. Moreover early treatment of UUO/CKD animals with an angiotensin-converting-enzyme inhibitor (ACE I), Enalapril, significantly attenuated cardiac fibrosis. Enalapril antagonized activation of the TGF-β signaling pathway in the UUO/CKD heart. In summary our study demonstrates the presence of pathological cardiac hypertrophy and fibrosis in mice early in UUO-induced CKD, in association with early activation of the TGF-β/Smad signaling pathway. We also demonstrate the beneficial effect of ACE I in alleviating this early fibrogenic process in the heart in UUO/CKD animals.

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Section: Methodsmentioning

confidence: 99%

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Ham

Jin

Lei

et al. 2018

Sci Rep

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show abstract

“…[4344] High levels of VEGF-A also lead to vascular permeability in the glomeruli,[45] Physiological levels of NO (nitric oxide) creates low vascular permeability but NO levels too high or too low can lead to hyper-permeability that in turn lead to glomerular injury and diabetic nephropathy. [39]…”

Section: Introductionmentioning

confidence: 99%

“…Abnormal angiogenesis in diabetes is mediated through VEGF-A family especially VEGF-A 164 and VEGF-A188 isoforms and VEGFR1 and VEGFR2 receptors. [ 43 44 ] High levels of VEGF-A also lead to vascular permeability in the glomeruli,[ 45 ] Physiological levels of NO (nitric oxide) creates low vascular permeability but NO levels too high or too low can lead to hyper-permeability that in turn lead to glomerular injury and diabetic nephropathy. [ 39 ]…”

Section: Introductionmentioning

confidence: 99%

Imbalance of angiogenesis in diabetic complications: The mechanisms

2012

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Type 2 diabetes mellitus is a complex disease and a chronic health-care problem. Nowadays, because of alteration of lifestyle such as lack of exercise, intake of high fat diet subsequently obesity and aging population, the prevalence of diabetes mellitus is increasing quickly in around the world. The international diabetes federation estimated in 2008, that 246 million adults in worldwide suffered from diabetes mellitus and the prevalence of disease is expected to reach to 380 million by 2025. Although, mainly in management of diabetes focused on hyperglycemia, however, it is documented that abnormalities of angiogenesis may contribute in the pathogenesis of diabetes complications. Angiogenesis is the generation of new blood vessels from pre-existing ones. Normal angiogenesis depends on the intricate balance between angiogenic factors (such as VEGF, FGF2, TGF-β, angiopoietins) and angiostatic factors (angiostatin, endostatin, thrombospondins). Vascular abnormalities in different tissues including retina and kidney can play a role in pathogenesis of micro-vascular complications of diabetes; also vascular impairment contributes in macrovascular complications e.g., diabetic neuropathy and impaired formation of coronary collaterals. Therefore, identifying of different mechanisms of the diabetic complications can give us an opportunity to prevent and/or treat the following complications and improves quality of life for patients and society. In this review, we studied the mechanisms of angiogenesis in micro-vascular and macro-vascular complications of diabetes mellitus.

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“…VEGFs exert their biological outcomes through their interaction with specific (VEGF-R) receptors [7]. Abnormal angiogenesis in diabetes is likely mediated in part by exuberant VEGF-A family-induced signaling, which induces diabetic retinopathy and nephropathy in diabetic patients [8][9][10]. Ang-1 supports endothelial cell survival, alleviates endothelial interactions with supporting cells, and controls vascular permeability [11].…”

mentioning

confidence: 99%

Diminished Circulating Levels of Angiogenic Factors and Rage Ligands in Helminth–Diabetes Comorbidity and Reversal Following Anthelmintic Treatment

Ray

Munisankar

Menon

et al. 2021

The Journal of Infectious Diseases

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Background Various epidemiological and experimental studies propose that helminths could play a preventive role against the progression of Type 2 diabetes mellitus (T2DM). T2DM induces microvascular and large vessel complications mediated by elevated levels of angiogenic factors and soluble RAGE ligands. However, the interactions between helminths and host angiogenic factors and RAGE ligands are unexplored. Methods To assess the relationship between a soil-transmitted helminth, Strongyloides stercoralis (Ss) and T2DM, we measured plasma levels of VEGF-A, C, D, Angio-1 and Angio-2 and their receptors VEGF-R1, R2 and R3 as well as sRAGE and their ligands AGE, S100A12 and HMBG-1 in individuals with T2DM with Ss+ or without Ss infection (Ss-). In Ss+ individuals, we also measured the levels of aforementioned factors 6 months following anthelmintic therapy. Results Ss+ individuals exhibited significantly decreased levels of VEGF-A, C, D, Angio-1 and Angio-2 and their soluble receptors VEGF-R1, R2 and R3, that increased following anthelmintic therapy. Likewise, Ss+ individuals exhibited significantly decreased levels of AGE and their ligands sRAGE, S100A12 and HMBG-1 which reversed following anthelmintic therapy. Conclusion Our data suggest that Ss infection could play a beneficial role by limiting or delaying the T2DM related vascular complications.

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Restoration of Angiogenesis by Enalapril in Diabetic Hindlimb Ischemc Rats

Cited by 4 publications

References 30 publications

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Imbalance of angiogenesis in diabetic complications: The mechanisms

Diminished Circulating Levels of Angiogenic Factors and Rage Ligands in Helminth–Diabetes Comorbidity and Reversal Following Anthelmintic Treatment

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