The multifaceted factor peroxisome proliferator-activated receptor γ (PPARγ) in metabolism, immunity, and cancer

Kim, Jung Hoon; Song, Jaewhan; Park, Kye Won

doi:10.1007/s12272-015-0559-x

Cited by 57 publications

(39 citation statements)

References 114 publications

(110 reference statements)

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“…However, afar of its adipose functions PPARG is also vital for development of some important organs such as heart and the placenta [11]. Although most research on PPARG has been focused on its metabolic action, some of them are neurogenesis, osteogenesis, cancer, or cardiovascular disease [14]. Such pleiotropism of actions gives us a clue of the relevance of this transcription factor regarding health and disease.…”

Section: The Pparg Physiologymentioning

confidence: 99%

Commonalities in the Association between PPARG and Vitamin D Related with Obesity and Carcinogenesis

2016

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The PPAR nuclear receptor family has acquired great relevance in the last decade, which is formed by three different isoforms (PPARα, PPARβ/δ, and PPAR ϒ). Those nuclear receptors are members of the steroid receptor superfamily which take part in essential metabolic and life-sustaining actions. Specifically, PPARG has been implicated in the regulation of processes concerning metabolism, inflammation, atherosclerosis, cell differentiation, and proliferation. Thus, a considerable amount of literature has emerged in the last ten years linking PPARG signalling with metabolic conditions such as obesity and diabetes, cardiovascular disease, and, more recently, cancer. This review paper, at crossroads of basic sciences, preclinical, and clinical data, intends to analyse the last research concerning PPARG signalling in obesity and cancer. Afterwards, possible links between four interrelated actors will be established: PPARG, the vitamin D/VDR system, obesity, and cancer, opening up the door to further investigation and new hypothesis in this fascinating area of research.

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Section: The Pparg Physiologymentioning

confidence: 99%

Commonalities in the Association between PPARG and Vitamin D Related with Obesity and Carcinogenesis

2016

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“…Pparγ is necessary and sufficient for adipogenesis [4]. Pparγ upstream regulators including CCAAT/enhancer binding protein (C/ebp), Early B cell factor, Interferon regulatory factor, Kruppel -like factor, early growth response, Inhibitor of DNA binding, Zinc finger proteins, and its downstream target genes have shown for their roles in lipid synthesis and adipocyte differentiation [5,6,7]. As Pparγ would be regulated by various integrated pathways, identification of a broader window of Pparγ upstream and its target genes linked to adipogenesis would provide further understanding of Pparγ and adipocyte biology.…”

Section: Introductionmentioning

confidence: 99%

Small Molecule-Induced Complement Factor D (Adipsin) Promotes Lipid Accumulation and Adipocyte Differentiation

et al. 2016

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Adipocytes are differentiated by various transcriptional cascades integrated on the master regulator, Pparγ. To discover new genes involved in adipocyte differentiation, preadipocytes were treated with three newly identified pro-adipogenic small molecules and GW7845 (a Pparγ agonist) for 24 hours and transcriptional profiling was analyzed. Four genes, Peroxisome proliferator-activated receptor γ (Pparγ), human complement factor D homolog (Cfd), Chemokine (C-C motif) ligand 9 (Ccl9), and GIPC PDZ Domain Containing Family Member 2 (Gipc2) were induced by at least two different small molecules but not by GW7845. Cfd and Ccl9 expressions were specific to adipocytes and they were altered in obese mice. Small hairpin RNA (shRNA) mediated knockdown of Cfd in preadipocytes inhibited lipid accumulation and expression of adipocyte markers during adipocyte differentiation. Overexpression of Cfd promoted adipocyte differentiation, increased C3a production, and led to induction of C3a receptor (C3aR) target gene expression. Similarly, treatments with C3a or C3aR agonist (C4494) also promoted adipogenesis. C3aR knockdown suppressed adipogenesis and impaired the pro-adipogenic effects of Cfd, further suggesting the necessity for C3aR signaling in Cfd-mediated pro-adipogenic axis. Together, these data show the action of Cfd in adipogenesis and underscore the application of small molecules to identify genes in adipocytes.

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“…AP is reported as a strong antioxidant that not only stifles the formation of ROS and free radical generation or augmentation of endogenous antioxidant enzymes but also modulates contractile function of heart and the survival or death signalling of ROS [36][37][38][39]. Flavonoids are also believed to play an important role in activation of PPARc which regulate the inflammatory response [40][41][42]. It is reported that PPARc may serve as a potential therapeutic target to prevent cardiac hypertrophy and heart failure in metabolic disorders [43,44].…”

Section: Introductionmentioning

confidence: 99%

Apigenin Attenuates β-Receptor-Stimulated Myocardial Injury Via Safeguarding Cardiac Functions and Escalation of Antioxidant Defence System

2015

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Apigenin (AP) is a flavone in dietary flavonoids reported as strong antioxidant and elite modulator of PPARγ. The current study evaluated the consequence of AP in isoproterenol (ISO)-induced oxidative stress and myocardial infarction during β-adrenergic receptor stimulus in rats by persistent hemodynamic, biochemical and histopathological changes. Rats received AP (25, 50 and 75 mg/kg/day) or vehicle i.p. for 14 days and ISO (100 mg/kg, s.c.) on 13th and 14th days for initiation of cardiotoxicity. ISO-treated rats showed evidence of significant dwindle in systolic and diastolic arterial pressures, maximal positive rate of developed left ventricular pressure. In totting up, a noteworthy diminution in activities of creatine kinase-MB isoenzyme, reduced glutathione, superoxide dismutase, catalase and level along with rise in malondialdehyde content were observed. The shielding function of AP on isoproterenol-induced myocardial damage was observed by attenuating all the endogenous parameters and the membrane-bound enzymes. It was confirmed by histopathological examinations. The effect of AP at the doses of 50 and 75 mg/kg showed added apparent than at the dose of 25 mg/kg. Current study thus provides confirmation for protective effects of AP on myocardium in experimentally induced myocardial infarction.

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The multifaceted factor peroxisome proliferator-activated receptor γ (PPARγ) in metabolism, immunity, and cancer

Cited by 57 publications

References 114 publications

Commonalities in the Association between PPARG and Vitamin D Related with Obesity and Carcinogenesis

Commonalities in the Association between PPARG and Vitamin D Related with Obesity and Carcinogenesis

Small Molecule-Induced Complement Factor D (Adipsin) Promotes Lipid Accumulation and Adipocyte Differentiation

Apigenin Attenuates β-Receptor-Stimulated Myocardial Injury Via Safeguarding Cardiac Functions and Escalation of Antioxidant Defence System

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