Peroxisome Proliferator-Activated Receptor α in Lipid Metabolism and Atherosclerosis

Yu, Xiaohua; Zheng, Xi-Long; Tang, Chao-Ke

doi:10.1016/bs.acc.2015.06.005

Cited by 61 publications

(35 citation statements)

References 150 publications

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“…Peroxisome proliferator-activated receptor α (PPARα) is an essential nuclear receptor that plays a critical role in lipid metabolism (i.e., fatty acid β-oxidation) and regulation of inflammation in various cell types and tissues [6][7][8]. Due to its regulation of macrophage-mediated inflammation, PPARα is a promising target for various human pathologies, particularly cardiovascular and metabolic diseases [9,10]. In addition, PPARα expression is involved in protective role against numerous disease models including acute lung injury [11], sepsis-associated acute kidney injury [12], non-alcoholic steatohepatitis [13], etc.…”

Section: Introductionmentioning

confidence: 99%

The Peroxisome Proliferator-Activated Receptor α- Agonist Gemfibrozil Promotes Defense Against Mycobacterium abscessus Infections

Kim

Hanh

et al. 2020

Cells

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Peroxisome proliferator-activated receptor α (PPARα) shows promising potential to enhance host defenses against Mycobacterium tuberculosis infection. Herein we evaluated the protective effect of PPARα against nontuberculous mycobacterial (NTM) infections. Using a rapidly growing NTM species, Mycobacterium abscessus (Mabc), we found that the intracellular bacterial load and histopathological damage were increased in PPARα-null mice in vivo. In addition, PPARα deficiency led to excessive production of proinflammatory cytokines and chemokines after infection of the lung and macrophages. Notably, administration of gemfibrozil (GEM), a PPARα activator, significantly reduced the in vivo Mabc load and inflammatory response in mice. Transcription factor EB was required for the antimicrobial response against Mabc infection. Collectively, these results suggest that manipulation of PPARα activation has promising potential as a therapeutic strategy for NTM disease.

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Section: Introductionmentioning

confidence: 99%

The Peroxisome Proliferator-Activated Receptor α- Agonist Gemfibrozil Promotes Defense Against Mycobacterium abscessus Infections

Kim

Hanh

et al. 2020

Cells

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“…6c). PPARα plays an important role in metabolic regulation and affects the different links of lipid metabolism, including fatty acid uptake, fatty acid activation, intracellular fatty acid binding, mitochondrial and peroxisomal fatty acid oxidation 22 . In the present study, we found that the expression level of PPARα gene was significantly decreased in the APFL group compared with the AP group.…”

Section: Discussionmentioning

confidence: 99%

RNA sequence analysis of rat acute experimental pancreatitis with and without fatty liver: a gene expression profiling comparative study

Wang

Yan

Wang

et al. 2017

Sci Rep

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Fatty liver (FL) is one of the risk factors for acute pancreatitis and is also indicative of a worse prognosis as compared to acute pancreatitis without fatty liver (AP). The aim of the present study was to analyze, at the hepatic level, the differentially expressed genes (DEGs) between acute pancreatitis with fatty liver (APFL) rats and AP rats. GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analyses of these DEGs indicated that PPARα signalling pathway and fatty acid degradation pathway may be involved in the pathological process of APFL, which indicated that fatty liver may aggravate pancreatitis through these pathways. Moreover, the excessive activation of JAK/STAT signaling pathway and toll-like receptor signaling pathway was also found in APFL group as shown in heat map. In conclusion, the inhibition of PPARα signaling pathway and the fatty acid degradation pathway may lead to the further disorder of lipid metabolism, which can aggravate pancreatitis.

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“…Peroxisome proliferator-activated receptor alpha and delta (PPAR α/δ) regulate lipid metabolism in liver and glucose homeostasis. 24 PPARα activation leads to control of lipid flux and, in the liver, inhibition of inflammatory genes induced by nuclear factor k-B and improvement of necro-inflammatory activity. 25 In addition, active PPARδ improves glucose homeostasis and inhibits hepatic lipogenesis, and has antiinflammatory activity in macrophages and Kupffer cells.…”

Section: Peroxisome Proliferator-activated Receptor (Ppar) Agonistsmentioning

confidence: 99%

The therapeutic landscape of non‐alcoholic steatohepatitis

Perazzo

Dufour

2016

Liver International

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Non-alcoholic steatohepatitis (NASH) is characterized by lobular inflammation and hepatocellular ballooning, and may be associated with liver fibrosis leading to cirrhosis and its complications. A pharmacological approach is necessary to treat NASH because of failure to change dietary habits and lifestyle in most patients. Insulin resistance with an increased release of free fatty acids, oxidative stress and activation of inflammatory cytokines seem to be key features for disease progression.

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Peroxisome Proliferator-Activated Receptor α in Lipid Metabolism and Atherosclerosis

Cited by 61 publications

References 150 publications

The Peroxisome Proliferator-Activated Receptor α- Agonist Gemfibrozil Promotes Defense Against Mycobacterium abscessus Infections

The Peroxisome Proliferator-Activated Receptor α- Agonist Gemfibrozil Promotes Defense Against Mycobacterium abscessus Infections

RNA sequence analysis of rat acute experimental pancreatitis with and without fatty liver: a gene expression profiling comparative study

The therapeutic landscape of non‐alcoholic steatohepatitis

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