The roles of PPARγ and its agonists in autoimmune diseases: A comprehensive review

Liu, Yu; Wang, Jiayu; Luo, Shuangyan; Zhan, Yi; Lu, Qianjin

doi:10.1016/j.jaut.2020.102510

Cited by 77 publications

(60 citation statements)

References 146 publications

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“…Different from corn overfeeding, the PPAR signaling pathway is highly enriched in the fructose and sucrose overfeeding groups. The PPAR pathway regulates lipid metabolism, participates in fat cell differentiation [21,22]. The liver-type fatty acid binding protein (FABP1) can speci cally bind to fatty acids and has a transport effect on fatty acids.…”

Section: Discussionmentioning

confidence: 99%

Study on The Effect of Different Type of Sugar on Lipid Deposition in Goose Fatty Liver

Wei¹,

Deng²,

Teng³

et al. 2021

Preprint

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Backgroud: Early research in our lab is indicated that the effect of glucose, fructose and sucrose on the levels of triacylglycerol and inflammatory factor was significantly different, and it is speculated that the regulatory mechanism of lipid deposition by different type of sugar in the liver is different. Methods: In order to explore lipid deposition difference mediated by different type of sugar (glucos, fructose and sucrose) in goose fatty liver formation, this experiment was performed from cell culture, overfeeding experiment and transcriptome analysis three level. Results: Cell culture experiment results indicated that the levels of intracellular triglyceride (TG), total cholesterol (T-CHO) and lipid content of fructose treatment and sucrose treatment were significantly higher than those of glucose treatment (P < 0.05). In slaughter performance, the liver weight, the ratio of liver weight to body weight, feed conversion ratio (liver weight / feed consumption ) were better in sucrose overfeeding group (P < 0.05). In addition, the liver of the sucrose overfeeding group contained a lot of unsaturated fatty acids, especially (n-3) polyunsaturated fatty acids (n-3 PUFA ) (P < 0.05). Transcriptome analysis shown that the PPAR signaling pathway is highly enriched in the fructose and sucrose overfeeding groups; cell cycle and DNA replication pathways were highly enriched in the glucose overfeeding group. Conclusions: Due to lipids outward transportation decrease and anti-imflammation of unsaturated fatty acids (UFA), thereby, fructose and sucrose hve better ability to induce steatosis in foie gras formation.

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Section: Discussionmentioning

confidence: 99%

Study on The Effect of Different Type of Sugar on Lipid Deposition in Goose Fatty Liver

Wei¹,

Deng²,

Teng³

et al. 2021

Preprint

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“…PPAR-γ heteromerizes with the retionid X-receptor and activates adiponectin expression. Contrary to expectations, in SARDs with high adiponectin serum levels, such as RA, low levels of PPAR-γ expression or activity is present and also beneficial effects of PPAR-γ activation have been demonstrated [ 160 , 161 ]. This indicates that adiponectin serum levels are elevated in these disorders for reasons other than PPAR-γ activation.…”

Section: Divergent Changes In the Activation Or Suppression Of Adiponectin Gene Regulation By Transcription Factors Can Affect Its Serum mentioning

confidence: 98%

“…In SLE, elevated PPAR-γ levels have been shown [ 162 ], but the beneficial effects of PPAR-γ activation have also been demonstrated in cell experiments and animal models [ 163 , 164 ]. The PPAR-γ activators TZDs (pioglitazone and rosiglitazone) are approved by the FDA for type 2 diabetes [ 165 ], but are thought to exert beneficial effects on SARDs with altered PPAR-γ activity [ 160 ]. Clinical trials with TZDs have been conducted in RA and in SLE patients, with the focus on inflammation control, cardiovascular protection and skeletal muscle dysfunction [ 165 ].…”

Section: Divergent Changes In the Activation Or Suppression Of Adiponectin Gene Regulation By Transcription Factors Can Affect Its Serum mentioning

confidence: 99%

“…PPAR-γ is the product of one gene, but has been reported to have 2 splice variants. While PPAR-γ1 is present in macrophages, colonic epithelium, endothelium and vascular smooth muscle cells, PPAR-γ2 is predominantly present in adipose tissue [ 160 ]. PPAR-γ expression is increased in adipogenesis and in monocytes, when transdifferentiating into macrophages [ 184 ].…”

Section: How Inflammatory Cytokines Il-6 and Tnf-α Regulate Adiponectin Levels In Sardsmentioning

confidence: 99%

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Adiponectin Deregulation in Systemic Autoimmune Rheumatic Diseases

Brezovec

Perdan-Pirkmajer

Čučnik

et al. 2021

IJMS

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Deregulation of adiponectin is found in systemic autoimmune rheumatic diseases (SARDs). Its expression is downregulated by various inflammatory mediators, but paradoxically, elevated serum levels are present in SARDs with high inflammatory components, such as rheumatoid arthritis and systemic lupus erythematosus. Circulating adiponectin is positively associated with radiographic progression in rheumatoid arthritis as well as with cardiovascular risks and lupus nephritis in systemic lupus erythematosus. However, in SARDs with less prominent inflammation, such as systemic sclerosis, adiponectin levels are low and correlate negatively with disease activity. Regulators of adiponectin gene expression (PPAR-γ, Id3, ATF3, and SIRT1) and inflammatory cytokines (interleukin 6 and tumor necrosis factor α) are differentially expressed in SARDs and could therefore influence total adiponectin levels. In addition, anti-inflammatory therapy could also have an impact, as tocilizumab treatment is associated with increased serum adiponectin. However, anti-tumor necrosis factor α treatment does not seem to affect its levels. Our review provides an overview of studies on adiponectin levels in the bloodstream and other biological samples from SARD patients and presents some possible explanations why adiponectin is deregulated in the context of therapy and gene regulation.

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“…Other study suggests that decreased INFG in patients with anxiety disorder is not a cause but a result of the disease[70]. However, all PPARs regulate its expression negatively via INFG promotor binding and blocking its transcriptional activity ([71][72][73][74][75], see supplementary). Thus, link between PPARs and INFG regulation is unequivocal, but determining if decreased INFG concentration is a disease's cause, or a consequence is a subject for further studies.…”

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confidence: 99%

Role of PPARs in Progression of Anxiety: Literature Analysis and Signaling Pathways Reconstruction

et al. 2020

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Peroxisome proliferator-activated receptor (PPAR) group includes three isoforms encoded by PPARG, PPARA, and PPARD genes. High concentrations of PPARs are found in parts of the brain linked to anxiety development, including hippocampus and amygdala. Among three PPAR isoforms, PPARG demonstrates the highest expression in CNS, where it can be found in neurons, astrocytes, and glial cells. Herein, the highest PPARG expression occurs in amygdala. However, little is known considering possible connections between PPARs and anxiety behavior. We reviewed possible connections between PPARs and anxiety. We used the Pathway Studio software (Elsevier). Signal pathways were created according to previously developed algorithms. SNEA was performed in Pathway Studio. Current study revealed 14 PPAR-regulated proteins linked to anxiety. Possible mechanism of PPAR involvement in neuroinflammation protection is proposed. Signal pathway reconstruction and reviewing aimed to reveal possible connection between PPARG and CCK-ergic system was conducted. Said analysis revealed that PPARG-dependent regulation of MME and ACE peptidase expression may affect levels of nonhydrolysed, i.e., active CCK-4. Impairments in PPARG regulation and following MME and ACE peptidase expression impairments in amygdala may be the possible mechanism leading to pathological anxiety development, with brain CCK-4 accumulation being a key link. Literature data analysis and signal pathway reconstruction and reviewing revealed two possible mechanisms of peroxisome proliferator-activated receptors involvement in pathological anxiety: (1) cytokine expression and neuroinflammation mechanism and (2) regulation of peptidases targeted to anxiety-associated neuropeptides, primarily CCK-4, mechanism.

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The roles of PPARγ and its agonists in autoimmune diseases: A comprehensive review

Cited by 77 publications

References 146 publications

Study on The Effect of Different Type of Sugar on Lipid Deposition in Goose Fatty Liver

Study on The Effect of Different Type of Sugar on Lipid Deposition in Goose Fatty Liver

Adiponectin Deregulation in Systemic Autoimmune Rheumatic Diseases

Role of PPARs in Progression of Anxiety: Literature Analysis and Signaling Pathways Reconstruction

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