Effects of rosiglitazone (<scp>PPAR</scp> <i>γ</i> agonist) on the myocardium in non‐hypertensive diabetic rats 罗格列酮（PPAR <i>γ</i> 激动剂）对非高血压糖尿病大鼠的心肌的影响

Abou-Daya, Khodor I.; Daya, Hussein Abu; Eddine, Mohamad Nasser; Nahhas, Georges J.; Nuwayri-Salti, Nuha

doi:10.1111/1753-0407.12140

Cited by 13 publications

(7 citation statements)

References 48 publications

(57 reference statements)

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“…PPARγ and its ligands have a wide spectrum of functions, regulating metabolism, attenuating inflammation, maintaining the balance of immune cells, inhibiting apoptosis and oxidative stress, and improving endothelial function ( 40 ). Results from different experimental models have shown that PPARγ and its ligands play a critical role in the regulation of various biological processes in the cardiovascular system under pathological conditions: they attenuate cardiac fibrosis in diabetic rats ( 41 , 42 ), and alleviate ischemia–reperfusion injury through the inhibition of inflammation, improve endothelial function, reduce oxidative, stress, and calcium overload in rabbits ( 43 ).…”

Section: Discussionmentioning

confidence: 99%

Treatment with a New Peroxisome Proliferator-Activated Receptor Gamma Agonist, Pyridinecarboxylic Acid Derivative, Increases Angiogenesis and Reduces Inflammatory Mediators in the Heart of Trypanosoma cruzi-Infected Mice

et al. 2017

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Trypanosoma cruzi infection induces an intense inflammatory response in diverse host tissues. The immune response and the microvascular abnormalities associated with infection are crucial aspects in the generation of heart damage in Chagas disease. Upon parasite uptake, macrophages, which are involved in the clearance of infection, increase inflammatory mediators, leading to parasite killing. The exacerbation of the inflammatory response may lead to tissue damage. Peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-dependent nuclear transcription factor that exerts important anti-inflammatory effects and is involved in improving endothelial functions and proangiogenic capacities. In this study, we evaluated the intermolecular interaction between PPARγ and a new synthetic PPARγ ligand, HP24, using virtual docking. Also, we showed that early treatment with HP24, decreases the expression of NOS2, a pro-inflammatory mediator, and stimulates proangiogenic mediators (vascular endothelial growth factor A, CD31, and Arginase I) both in macrophages and in the heart of T. cruzi-infected mice. Moreover, HP24 reduces the inflammatory response, cardiac fibrosis and the levels of inflammatory cytokines (TNF-α, interleukin 6) released by macrophages of T. cruzi-infected mice. We consider that PPARγ agonists might be useful as coadjuvants of the antiparasitic treatment of Chagas disease, to delay, reverse, or preclude the onset of heart damage.

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Section: Discussionmentioning

confidence: 99%

Treatment with a New Peroxisome Proliferator-Activated Receptor Gamma Agonist, Pyridinecarboxylic Acid Derivative, Increases Angiogenesis and Reduces Inflammatory Mediators in the Heart of Trypanosoma cruzi-Infected Mice

et al. 2017

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“…They are used as insulin sensitizers to control hyperglycemia in type 2 diabetes (Tontonoz & Spiegelman, ) and to protect kidneys from diabetic and nondiabetic injuries by reducing microalbuminuria (Bakris et al, ; Sarafidis, Stafylas, Georgianos, Saratzis, & Lasaridis, ; Sugawara et al, ). Rosiglitazone has also been found to have a cardioprotective effect upon the cardiac muscle in the diabetic rat model (Abou Daya, Abu Daya, Nasser Eddine, Nahhas, & Nuwayri‐Salti, ; Yue et al, ). However, the exact mechanism of how rosiglitazone act as a cardio‐ or renoprotective is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Effect of hyperglycemia and rosiglitazone on renal and urinary neprilysin indb/dbdiabetic mice

et al. 2020

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Alteration in renin‐angiotensin system (RAS) has been implicated in the pathophysiology of diabetic kidney disease (DKD). The deleterious actions of angiotensin II (Ang II) could be antagonized by the formation of Ang‐(1–7), generated by the actions of angiotensin‐converting enzyme 2 (ACE2) and neprilysin (NEP). NEP degrades several peptides, including natriuretic peptides, bradykinin, amyloid beta, and Ang I. Although combination of Ang II receptor and NEP inhibitor treatment benefits patients with heart failure, the role of NEP in renal pathophysiology is a matter of active research. NEP pathway is a potent enzyme in Ang I to Ang‐(1–7) conversion in the kidney of ACE2‐deficient mice, suggesting a renoprotective role of NEP. The aim of the study is to test the hypothesis that chronic hyperglycemia downregulates renal NEP protein expression and activity in db/db diabetic mice and treatment with rosiglitazone normalizes hyperglycemia, renal NEP expression, and attenuates albuminuria. Mice received rosiglitazone (20 mg kg−1 day−1) for 10 weeks. Western blot analysis, immunohistochemistry, and enzyme activity revealed a significant decrease in renal and urinary NEP expression and activity in 16‐wk db/db mice compared with lean control (p < .0001). Rosiglitazone also attenuated albuminuria and increased renal and urinary NEP expressions (p < .0001). In conclusion, data support the hypothesis that diabetes decreases intrarenal NEP, which could have a pivotal role in the pathogenesis of DKD. Urinary NEP may be used as an index of intrarenal NEP status. The renoprotective effects of rosiglitazone could be mediated by upregulation of renal NEP expression and activity in db/db diabetic mice.

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“…Because of different transcript, translation, and tissue distribution, each protein has different biological functions in a variety of organs and cells ( Table 1 ) [ 13 ]. So it is not a surprise that PPAR γ plays important roles in CVDs including hypertension [ 17 , 24 , 25 ], atherosclerosis [ 26 ], HF [ 27 ], diabetic cardiomyopathy [ 11 , 28 ], angiogenesis [ 29 ], valvular calcification [ 30 ], aortic aneurysm [ 31 ], restenosis following cardiovascular interventions [ 32 ], and ischemia/reperfusion (I/R) injury [ 33 , 34 ].…”

Section: Structure and Function Of Ppar γmentioning

confidence: 99%

“…Interestingly, peroxisome proliferator-activated receptor- γ (PPAR γ ) has been identified to have the function of antimyocardial fibrosis [ 9 – 11 ]. According to published investigations, PPAR γ has a wide spectrum of functions in regulating metabolism, attenuating inflammation, maintaining the balance of immune cells, inhibiting apoptosis and oxidative stress, and improving endothelial function [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor-γIs Critical to Cardiac Fibrosis

et al. 2016

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Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-activated transcription factor belonging to the nuclear receptor superfamily, which plays a central role in regulating lipid and glucose metabolism. However, accumulating evidence demonstrates that PPARγ agonists have potential to reduce inflammation, influence the balance of immune cells, suppress oxidative stress, and improve endothelial function, which are all involved in the cellular and molecular mechanisms of cardiac fibrosis. Thus, in this review we discuss the role of PPARγ in various cardiovascular conditions associated with cardiac fibrosis, including diabetes mellitus, hypertension, myocardial infarction, heart failure, ischemia/reperfusion injury, atrial fibrillation, and several other cardiovascular disease (CVD) conditions, and summarize the developmental status of PPARγ agonists for the clinical management of CVD.

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Effects of rosiglitazone (PPAR γ agonist) on the myocardium in non‐hypertensive diabetic rats 罗格列酮（PPAR γ 激动剂）对非高血压糖尿病大鼠的心肌的影响

Abstract: Rosiglitazone, in combination with even sub-optimal doses of insulin therapy, has protective effects on cardiac muscle in diabetic animals especially those expressed as muscle hypertrophy, muscle cell death, and fibrosis.

Cited by 13 publications

References 48 publications

Treatment with a New Peroxisome Proliferator-Activated Receptor Gamma Agonist, Pyridinecarboxylic Acid Derivative, Increases Angiogenesis and Reduces Inflammatory Mediators in the Heart of Trypanosoma cruzi-Infected Mice

Treatment with a New Peroxisome Proliferator-Activated Receptor Gamma Agonist, Pyridinecarboxylic Acid Derivative, Increases Angiogenesis and Reduces Inflammatory Mediators in the Heart of Trypanosoma cruzi-Infected Mice

Effect of hyperglycemia and rosiglitazone on renal and urinary neprilysin indb/dbdiabetic mice

Peroxisome Proliferator-Activated Receptor-γIs Critical to Cardiac Fibrosis

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