The peroxisome proliferator-activated receptor gamma (PPARγ) is highly expressed in human heart ventricles

Mehrabi, Mohammad Reza; Thalhammer, Theresia; Haslmayer, Petra; Glogar, Helmut D.; Wieselthaler, Georg; Humpeler, Susanne; Marktl, Wolfgang; Ekmekçioğlu, Cem

doi:10.1016/s0753-3322(02)00251-2

Cited by 14 publications

(14 citation statements)

References 20 publications

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“…Although the expression of PPARγ in cardiac myocytes is low compared with adipocytes, PPARγ ligands seem to act on cardiac myocytes. 7,44 We demonstrated that PPARγ ligands inhibited the cardiac expression of TNF-α at the transcriptional level, in part by antagonizing NF-κB activity. 7 Because TNF-α expression is elevated in the failing heart and has a negative inotropic effect on cardiac myocytes, treatment with PPARγ ligands may prevent the development of congestive heart failure.…”

Section: Pparγ and Ischemic Heart Diseasementioning

confidence: 94%

Peroxisome Proliferator-Activated Receptor .GAMMA. and Cardiovascular Diseases

Takano

Komuro

2009

Circ J

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Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor superfamily and form heterodimers with retinoid X receptor. Three PPAR isoforms have been isolated and termed α, β (or δ) and γ. Although PPARγ is expressed predominantly in adipose tissue and associated with adipocyte differentiation and glucose homeostasis, PPARγ is also present in a variety of cell types. Synthetic antidiabetic thiazolidinediones (TZDs) are well known as ligands and activators for PPARγ. After it was reported that activation of PPARγ suppressed production of pro-inflammatory cytokines in activated macrophages, medical interest in PPARγ has grown and there has been a huge research effort. PPARγ is currently known to be implicated in various human chronic diseases such as diabetes mellitus, atherosclerosis, rheumatoid arthritis, inflammatory bowel disease, and Alzheimer's disease. Many studies suggest that TZDs not only ameliorate insulin sensitivity, but also have pleiotropic effects on many tissues and cell types. Although activation of PPARγ seems to have beneficial effects on cardiovascular diseases, the mechanisms by which PPARγ ligands prevent their development are not fully understood. Recent data about the actions and its mechanisms of PPARγ-dependent pathway in cardiovascular diseases are discussed here. (Circ J 2009; 73: 214 -220)

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Section: Pparγ and Ischemic Heart Diseasementioning

confidence: 94%

Peroxisome Proliferator-Activated Receptor .GAMMA. and Cardiovascular Diseases

Takano

Komuro

2009

Circ J

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“…Initially, PPARγ was found mainly in adipocytes to regulate adipocyte differentiation and lipid metabolism and improve insulin sensitivity, and thus is closely related to hypertension, obesity, type II diabetes, insulin resistance, atherosclerosis and other metabolic syndromes (Cheang, Fang, & Tian, 2013;Jung, Torrejon, Chang, et al, 2012;Liu, Tian, Mao, et al, 2012;Rangwala, Rhoades, Shapiro, et al, 2003;Ryan, Didion, Mathur, et al, 2004;Way, Görgün, Tong, et al, 2001). Recently, however, PPARγ was also observed being expressed in the heart, vascular smooth muscle cells, endothelial cells and other parts (Hsueh, Jackson, & Law, 2001;Mehrabi, Thalhammer, Haslmayer, et al, 2002). In addition, PPARγ-activation agents, troglitazone, pioglitazone, and rosiglitazone, could inhibit angiotensin II-induced hypertrophy of neonatal rat cardiac myocytes (Hsueh et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

PPARγ–PI3K/AKT–NO signal pathway is involved in cardiomyocyte hypertrophy induced by high glucose and insulin

Peng

Chen

et al. 2015

Journal of Diabetes and its Complications

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“…Several studies have shown that PPARγ is expressed in healthy human coronary arteries, aortic vascular smooth muscle (VSM) cells and heart ventricles. 11, 12 Babaev et al found that conditional knockout of macrophage PPARγ increases atherosclerosis in C57BL/6 (macrophagespecific PPAR gamma knockout mice) and low-density lipoprotein receptor-deficient mice, 13 Adil et al, 14 realized that cardiac and aortic PPARγ expression is modulated by hypertension and oxidative stress in chronically glucosefed rats. Abundant evidences suggest that PPARγ agonists exert cardiovascular antioxidant and anti-inflammatory effects.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Chen¹,

Bing²,

He³

et al. 2009

Clinical Cardiology

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Background: Numerous evidence has suggested that either hypertension or atrial fibrillation (AF) is associated with systemic inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) has been proved to have anti-inflammatory effects and is implicated as a molecular pathway involved in many cardiovascular diseases, such as hypertension. The correlation between PPARγ inflammation and AF is still unknown. Methods: Using a case-control study design, 57 patients with hypertensive AF (persistent AF: 32, paroxysmal AF: 25) were included into the study groups. A total of 32 age-matched patients with hypertension, but without AF were selected as the control group. The expressions of PPARγ, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) mRNA in monocytes were detected by using a reverse transcription-polymerase chain reaction (RT-PCR). Interleukin-1 (IL-1) was measured by immunoenzymetric methods. Results: The PPARγ mRNA was markedly decreased in the hypertensive AF group as compared with the hypertensive non-AF group, and it was significantly lower in persistent AF than paroxysmal AF (0.222 ± 0.0702 vs 0.564 ± 0.0436, P<0.01). TNF-α mRNA, IL-6 mRNA, and IL-1 were increased in patients with hypertensive AF compared to the non-AF group and it was even higher in persistent AF than in paroxysmal AF (0.721 ± 0.0541 vs 0.530 ± 0.0496, 0.567 ± 0.044 vs 0.457 ± 0. 0505, 325.61 ± 88.10 vs 190.65 ± 59.38, respectively, P<0.01). TNF-α, IL-6, and IL-1 were in negative correlation with PPARγ, the correlation coefficient was −0.854, −0.769, and −0.702, respectively (P<0.01). Conclusions: In hypertensive patients, increased inflammatory cytokines were associated with increased incidence of AF and atrial remodeling; PPARγ may be involved in the pathogenesis of AF by regulation of inflammation.

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The peroxisome proliferator-activated receptor gamma (PPARγ) is highly expressed in human heart ventricles

Cited by 14 publications

References 20 publications

Peroxisome Proliferator-Activated Receptor .GAMMA. and Cardiovascular Diseases

Peroxisome Proliferator-Activated Receptor .GAMMA. and Cardiovascular Diseases

PPARγ–PI3K/AKT–NO signal pathway is involved in cardiomyocyte hypertrophy induced by high glucose and insulin

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

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