Ligand Activation of Peroxisome Proliferator–Activated Receptor β/δ (PPARβ/δ) Attenuates Carbon Tetrachloride Hepatotoxicity by Downregulating Proinflammatory Gene Expression
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Peroxisome proliferator-activated receptor (PPAR) beta/delta-null mice exhibit exacerbated hepatotoxicity in response to administration of carbon tetrachloride (CCl(4)). To determine whether ligand activation of the receptor protects against chemical toxicity in the liver, wild-type and PPARbeta/delta-null mice were administered CCl(4) with or without coadministration of the highly specific PPARbeta/delta ligand GW0742. Biomarkers of liver toxicity, including serum alanine aminotransferase (ALT) and hepatic tumor necrosis factor (TNF) alpha mRNA, were significantly higher in CCl(4)-treated PPARbeta/delta-null mice compared to wild-type mice. Hepatic expression of TNF-like weak inducer of apoptosis receptor (TWEAKr) and S100 calcium-binding protein A6 (S100A6/calcyclin), genes involved in nuclear factor kappa B signaling, was higher in the CCl(4)-treated PPARbeta/delta-null mice compared to wild-type mice. GW0742 treatment resulted in reduced serum ALT concentration and lower expression of CCl(4)-induced TNF-alpha, S100A6, monocyte chemoattractant protein-1 (MCP1), and TWEAKr in wild-type mice, and these effects were not observed in PPARbeta/delta-null mice. Expression of TNF-alpha was higher in PPARbeta/delta-null primary hepatocytes in response to interleukin-1beta treatment compared to wild-type hepatocytes, but GW0742 did not significantly modulate TNF-alpha expression in hepatocytes from either genotype. While PPARbeta/delta-null hepatic stellate exhibited higher rates of proliferation compared to wild-type cells, GW0742 did not affect alpha-smooth muscle actin expression in these cells. Combined, these findings demonstrate that ligand activation of PPARbeta/delta protects against chemically induced hepatotoxicity by downregulating expression of proinflammatory genes. Hepatocytes and hepatic stellate cells do not appear to directly mediate the inhibitory effects of ligand activation of PPARbeta/delta in liver, suggesting the involvement of paracrine and autocrine events mediated by hepatic cells.
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The PPAR-δ agonist GW0742 reduces hepatotoxicity by downregulating pro-inflammatory genes in a CCl4 mouse model via modulation of NF-κB signaling.
“the PPAR-δ agonist GW0742 was able to reduce hepatoxicity by downregulating the expression of pro-inflammatory genes in a CCl 4 mouse model via the modulation of NF-κB signaling.[146]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [146]
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Self-citationInterleukin‐1β induction of TNF‐α gene expression: Involvement of protein kinase C
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PPARβ agonists trigger neuronal differentiation in the human neuroblastoma cell line SH‐SY5Y
Loreto, S. D., D’Angelo, B., D’Amico, M. A., Benedetti, E., Cristiano, L., Cinque, B., Cifone, M. G., Cerù, M. P., Festuccia, C., & Cimini, A. (2007) · Journal of Cellular Physiology · doi:10.1002/jcp.20996 · Cited by 50 · see citing works
PPARβ/δ Protects Against Experimental Colitis Through a Ligand-Independent Mechanism
Hollingshead, H. E., Morimura, K., Adachi, M., Kennett, M. J., Billin, A. N., Willson, T. M., Gonzalez, F. J., & Peters, J. M. (2007) · Digestive Diseases and Sciences · doi:10.1007/s10620-006-9644-9 · Cited by 48 · see citing works
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Isoform specific changes in PPARα and β in colon and breast cancer with differentiation
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PPARβ-mediated growth suppression of baicalein and dexamethasone in human myeloma cells
Otsuyama, K.-I., Ma, Z., Abroun, S., Amin, J., Shamsasenjan, K., Asaoku, H., & Kawano, M. M. (2006) · Leukemia · doi:10.1038/sj.leu.2404462 · Cited by 24 · see citing works
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Self-citationVosper, H., Khoudoli, G. A., & Palmer, C. N. (2003) · Nuclear Receptor · doi:10.1186/1478-1336-1-9 · Cited by 21 · see citing works
Recent Advances in Peroxisome Proliferator- Activated Receptor Science
Shearer, B. G., & Hoekstra, W. J. (2005) · Frontiers in Medicinal Chemistry - Online · doi:10.2174/1567204052930970 · Cited by 13 · see citing works
Dyrøy, E., Røst, T. H., Pettersen, R. J., Halvorsen, B. L., Gudbrandsen, O. A., Ueland, T., Muna, Z. A., Müller, F., Nordrehaug, J. E., Aukrust, P., et al. (2006) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000255950.70774.d5 · Cited by 12 · see citing works
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- Takata, Y., Liu, J., Yin, F., Collins, A. R., Lyon, C. J., Lee, C. H., Atkins, A. R., Downes, M., Barish, G. D., Evans, R. M., et al . (2008). PPARdelta-mediated antiinflammatory mechanisms inhibit angiotensin IIaccelerated atherosclerosis. Proc. Natl. Acad. Sci. U.S.A. 105, 4277-4282.
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Sorted by citations
PPARs in Obesity-Induced T2DM, Dyslipidaemia and NAFLD
Gross, B., Pawlak, M., Lefebvre, P., & Staels, B. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.135 · Cited by 778 · see citing works
The role of Peroxisome Proliferator-Activated Receptors (PPAR) in immune responses
Christofides, A., Konstantinidou, E., Jani, C., & Boussiotis, V. (2020) · Metabolism: Clinical and Experimental · doi:10.1016/j.metabol.2020.154338 · Cited by 654 · see citing works
The role of peroxisome proliferator-activated receptors in carcinogenesis and chemoprevention
Peters, J. M., Shah, Y. M., & Gonzalez, F. J. (2012) · Nature reviews. Cancer · doi:10.1038/nrc3214 · Cited by 494 · see citing works
Self-citationPathophysiology and Mechanisms of Nonalcoholic Fatty Liver Disease.
Haas, J., Francque, S., & Staels, B. (2016) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021115-105331 · Cited by 372 · see citing works
PPARα: Energy Combustion, Hypolipidemia, Inflammation and Cancer
Pyper, S. R., Viswakarma, N., Yu, S., & Reddy, J. K. (2010) · Nuclear Receptor Signaling · doi:10.1621/nrs.08002 · Cited by 381 · see citing works
Omiecinski, C. J., Heuvel, J. P. V., Perdew, G. H., & Peters, J. M. (2010) · Toxicological Sciences · doi:10.1093/toxsci/kfq338 · Cited by 367 · see citing works
“This has been observed in a number of models including nonalcoholic steatohepatitis and chemically induced liver toxicity (Nagasawa et al., 2006; Shan et al., 2008a,b).”
BackgroundSelf-citationFrancque, S., Verrijken, A., Caron, S., Prawitt, J., Paumelle, R., Derudas, B., Lefèbvre, P., Taskinen, M., Hul, W. V., Mertens, I. L., et al. (2015) · Journal of Hepatology · doi:10.1016/j.jhep.2015.02.019 · Cited by 357 · see citing works
Roles of PPARs in NAFLD: Potential therapeutic targets
Tailleux, A., Wouters, K., & Staels, B. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2011.10.016 · Cited by 283 · see citing works
Nuclear receptors and nonalcoholic fatty liver disease
Cave, M. C., Clair, H. B., Hardesty, J., Falkner, K. C., Feng, W., Clark, B. J., Sidey, J., Shi, H., Aqel, B. A., McClain, C. J., et al. (2016) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2016.03.002 · Cited by 280 · see citing works
PPARs and nonalcoholic fatty liver disease
Liss, K. H. H., & Finck, B. N. (2016) · Biochimie · doi:10.1016/j.biochi.2016.11.009 · Cited by 275 · see citing works
“While treatment with GW0742 resulted in improvement in fibrosis in wild type mice, this effect was not seen in PPARδ null mice demonstrating a PPARδ-dependent mechanism of action to alleviate fibrosis in response to this stimulus [60,61].”
BackgroundTargeting nuclear receptors for the treatment of fatty liver disease
Tanaka, N., Aoyama, T., Kimura, S., & Gonzalez, F. J. (2017) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.05.011 · Cited by 212 · see citing works
Self-citationPhysiological functions of peroxisome proliferator-activated receptor β
Neels, J. G., & Grimaldi, P. A. (2014) · Physiological Reviews · doi:10.1152/physrev.00027.2013 · Cited by 161 · see citing works
Protection from liver fibrosis by a peroxisome proliferator-activated receptor δ agonist
Iwaisako, K., Haimerl, M., Paik, Y.-H., Taura, K., Kodama, Y., Sirlin, C., Yu, E., Yu, R. T., Downes, M., Evans, R. M., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1202464109 · Cited by 157 · see citing works
Sanderson, L. M., Boekschoten, M. V., Desvergne, B., Müller, M. M., & Kersten, S. (2009) · Physiological Genomics · doi:10.1152/physiolgenomics.00127.2009 · Cited by 144 · see citing works
Fougerat, A., Montagner, A., Loiseau, N., Guillou, H., & Wahli, W. (2020) · Cells · doi:10.3390/cells9071638 · Cited by 143 · see citing works
Emerging roles of peroxisome proliferator-activated receptor-β/δ in inflammation
Bishop‐Bailey, D., & Byström, J. (2009) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2009.06.011 · Cited by 120 · see citing works
“PPARβ/δ ligands also show promise in more chronic inflammatory models including those of hepatotoxicity (Shan et al., 2008), and experimental autoimmuneencephalomyelitis (Polaket al., 2005).17day administration of carbon tetrachloride results in a high level of liver toxicity accompanied by…”
BackgroundTranscriptional regulation of hepatic stellate cells
Mann, J., & Mann, D. A. (2009) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2009.03.011 · Cited by 119 · see citing works
“However it is reported that PPARβ/δ knockout HSC proliferates faster than wild-type HSC, which is in disagreement with the findings of the previously mentioned study [138].”
ResultTreating NASH by targeting peroxisome proliferator-activated receptors
Staels, B., Butruille, L., & Francque, S. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.07.004 · Cited by 110 · see citing works
Comparative Gene Expression Profiles Induced by PPARγ and PPARα/γ Agonists in Human Hepatocytes
Rogue, A., Lambert, C. B., Jossé, R., Anthérieu, S., Spire, C., Claude, N., & Guillouzo, A. (2011) · PLoS ONE · doi:10.1371/journal.pone.0018816 · Cited by 105 · see citing works
Cariello, M., Piccinin, E., & Moschetta, A. (2021) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2021.01.012 · Cited by 103 · see citing works
Peters, J. M., & Gonzalez, F. J. (2009) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2009.06.002 · Cited by 96 · see citing works
Self-citationHepatic PPARs: Their Role in Liver Physiology, Fibrosis and Treatment
Zardi, E. M., Navarini, L., Sambataro, G., Piccinni, P., Sambataro, F., Spina, C., & Dobrina, A. (2013) · Current Medicinal Chemistry · doi:10.2174/09298673113209990136 · Cited by 91 · see citing works
“PPAR / is expressed in quiescent HSCs, and especially in activated HSCs in vitro and in vivo but its role is not completely clear yet; indeed PPAR / favors HSCs proliferation but also counterbalances this effect expressing genes involved in esterification of vitamin A (2) and downregulating proinflammatory gene expres…”
BackgroundSilva, A. S., & Peixoto, C. (2018) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-018-2838-4 · Cited by 85 · see citing works
PPARs as Metabolic Sensors and Therapeutic Targets in Liver Diseases
Monroy-Ramírez, H. C., Galicia‐Moreno, M., Sandoval-Rodriguez, A. S., Meza-Ríos, A., Santos, A., & Armendáriz‐Borunda, J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22158298 · Cited by 86 · see citing works
“Lastly, it has been shown that PPARβ/δ has hepatoprotective effects modulating NF-κB signaling, consequently attenuating CCl4 hepatotoxicity [81].”
BackgroundKostadinova, R., Montagner, A., Gouranton, E., Fleury, S., Guillou, H., Dombrowicz, D., Desreumaux, P., & Wahli, W. (2012) · Cell & Bioscience · doi:10.1186/2045-3701-2-34 · Cited by 83 · see citing works
“In contrast, other studies concluded that GW0742- or KD3010-activated PPARβ/ δ attenuated CCl4-induced hepatotoxicity [13,15].”
BackgroundResultPeroxisome Proliferator-Activated Receptors and Their Agonists in Nonalcoholic Fatty Liver Disease
Choudhary, N. S., Kumar, N., & Duseja, A. K. (2019) · Journal of Clinical and Experimental Hepatology · doi:10.1016/j.jceh.2019.06.004 · Cited by 74 · see citing works
“Newer selective PPARa-specific agonists, known as selective PPARamodulators, are in different phases of development.35,36 N A FL D PPARb/d AND ITS AGONISTS PPARb/d is the least studied among all the PPAR isotypes, although it has significant expression in tissues controlling lipid metabolism, such as adipocytes, heart…”
MethodKořínková, L., Pražienková, V., Černá, L., Karnošová, A., Železná, B., Kuneš, J., & Maletı́nská, L. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.597583 · Cited by 68 · see citing works
Mehmood, A., Zhao, L., Wang, Y., Pan, F., Hao, S., Zhang, H., Iftikhar, A., & Usman, M. A. (2021) · Food Research International · doi:10.1016/j.foodres.2021.110180 · Cited by 67 · see citing works
Peters, J. M., Foreman, J. E., & Gonzalez, F. J. (2011) · Cancer and Metastasis Reviews · doi:10.1007/s10555-011-9320-1 · Cited by 61 · see citing works
Self-citationInsights into the Role of PPARβ/δ in NAFLD
Chen, J., Montagner, A., Tan, N. S., & Wahli, W. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19071893 · Cited by 60 · see citing works
Pharmacological agents for NASH
Ratziu, V. (2013) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2013.193 · Cited by 59 · see citing works
Lipids as targets for novel anti-inflammatory therapies
Huwiler, A., & Pfeilschifter, J. M. (2009) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2009.06.008 · Cited by 57 · see citing works
PPARβ/δ directs the therapeutic potential of mesenchymal stem cells in arthritis
Luz‐Crawford, P., Ipseiz, N., Espinosa-Carrasco, G., Caicedo, A., Téjédor, G., Toupet, K., Loriau, J., Scholtysek, C., Stoll, C., Khoury, M., et al. (2016) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2015-208696 · Cited by 57 · see citing works
Mechanisms of Action of Dehydroepiandrosterone
Clark, B. J., Prough, R. A., & Klinge, C. M. (2018) · Vitamins and hormones · doi:10.1016/bs.vh.2018.02.003 · Cited by 56 · see citing works
Sharma, S. K., Rana, S., Patial, V., Gupta, M., Bhushan, S., & Padwad, Y. S. (2016) · Human & Experimental Toxicology · doi:10.1177/0960327115627689 · Cited by 49 · see citing works
Zarei, M., Aguilar-Recarte, D., Palomer, X., & Vázquez‐Carrera, M. (2020) · Metabolism · doi:10.1016/j.metabol.2020.154342 · Cited by 49 · see citing works
Xu, E. G., Mager, E., Grosell, M., Hazard, E., Hardiman, G., & Schlenk, D. (2017) · Scientific Reports · doi:10.1038/srep44546 · Cited by 46 · see citing works
Nuclear receptors in liver fibrosis
Königshofer, P., Brusilovskaya, K., Petrenko, O., Hofer, B. S., Schwabl, P., Trauner, M., & Reiberger, T. (2021) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2021.166235 · Cited by 45 · see citing works
Zhao, T. M., Zhu, Y., Zhao, R., Xiong, S., Sun, J., Zhang, J., Fan, D., Deng, J., & Yang, H. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106820 · Cited by 39 · see citing works
Singh, A., & Chaudhary, R. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.114616 · Cited by 39 · see citing works
Current and emerging therapeutic landscape for metabolic dysfunction-associated steatohepatitis
Li, W., Alazawi, W., & Loomba, R. S. (2025) · The Lancet. Gastroenterology & hepatology · doi:10.1016/s2468-1253(25)00260-2 · Cited by 43 · see citing works
Foreman, J. E., Sorg, J. M., McGinnis, K. S., Rigas, B., Williams, J. L., Clapper, M. L., Gonzalez, F. J., & Peters, J. M. (2009) · Molecular Carcinogenesis · doi:10.1002/mc.20546 · Cited by 37 · see citing works
“high-density lipoprotein cholesterol [5], increase running endurance synergistically with exercise by increasing oxidative myofibers [6], prevent liver toxicity and fatty liver [7,8], and induce terminal”
BackgroundSelf-citationChen, J., Qin, X., Chen, M., Chen, T., Chen, Z., & He, B. (2024) · Pharmacological Research · doi:10.1016/j.phrs.2024.107124 · Cited by 36 · see citing works
GW0742, A HIGH-AFFINITY PPAR -β/δ AGONIST, INHIBITS ACUTE LUNG INJURY IN MICE
Paola, R. D., Crisafulli, C., Mazzon, E., Esposito, E., Paterniti, I., Galuppo, M., Genovese, T., Thiemermann, C., & Cuzzocrea, S. (2010) · Shock · doi:10.1097/shk.0b013e3181b8f2fb · Cited by 36 · see citing works
PPARβ Regulates Liver Regeneration by Modulating Akt and E2f Signaling
Liu, H., Fang, Y., Hu, Y. C., Gonzalez, F. J., Fang, J., & Wan, Y. Y. (2013) · PLoS ONE · doi:10.1371/journal.pone.0065644 · Cited by 34 · see citing works
Self-citationBility, M. T., Zhu, B., Kang, B. H., Gonzalez, F. J., & Peters, J. M. (2009) · Toxicological Sciences · doi:10.1093/toxsci/kfp212 · Cited by 34 · see citing works
“…notably those associated with inflammation (e.g., tumor necrosis factor-a, monocyte chemoattractant protein), and in doing so mediates anti-inflammatory activities via interfering with other transcription factors such as nuclear factor-jB (NF-jB) (Kilgore and Billin, 2008; Shan et al., 2008a,b).”
BackgroundSelf-citationCell metabolism-based therapy for liver fibrosis, repair, and hepatocellular carcinoma
Gilgenkrantz, H., Paradis, V., & Lotersztajn, S. (2023) · Hepatology · doi:10.1097/hep.0000000000000479 · Cited by 32 · see citing works
“[112,113]”
Preservation of basal AcSDKP attenuates carbon tetrachloride-induced fibrosis in the rat liver
Chen, Y., Liu, B., Zhang, Y., Chen, Y., Dong, G.-F., Ding, X.-D., Xu, L., Pat, B., Fan, J.-G., & Li, D. (2010) · Journal of Hepatology · doi:10.1016/j.jhep.2010.03.027 · Cited by 32 · see citing works
“Following leukocyte infiltration, proinflammatory cytokines and oxidative stress increase, inducing hepatocyte damage directly or by interrupting hepatocyte metabolism though suppression of cytochrome P450 and other genes [25,27].”
BackgroundMA, S.-C., ZHANG, H.-P., KONG, F.-Q., Zhang, H., Yang, C., HE, Y.-Y., Wang, Y., Yang, A., Tian, J., YANG, X.-L., et al. (2016) · Molecular Medicine Reports · doi:10.3892/mmr.2016.5120 · Cited by 32 · see citing works
Zhang, M., Barroso, E., Peña, L., Rada, P., Valverde, Á. M., Wahli, W., Palomer, X., & Vázquez‐Carrera, M. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.117303 · Cited by 31 · see citing works
“The protective effects of GW0742 have not been observed with hepatocytes and HSCs suggesting that paracrine and autocrine events mediated by different cells are involved [25].”
BackgroundMethodInfluentialKadayat, T. M., Shrestha, A., Jeon, Y. H., An, H., Kim, J., Cho, S. J., & Chin, J. (2020) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.9b01882 · Cited by 26 · see citing works
Zhu, B., Bai, R., Kennett, M. J., Kang, B.-H., Gonzalez, F. J., & Peters, J. M. (2010) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-10-0820 · Cited by 23 · see citing works
Self-citationTardiff, R. G., Carson, M. L., Sweeney, L. M., Kirman, C. R., Tan, Y., Andersen, M. E., Bevan, C. D., & Gargas, M. L. (2009) · Food and Chemical Toxicology · doi:10.1016/j.fct.2009.07.016 · Cited by 23 · see citing works
“…and peroxisome proliferation; PPARb/d plays a role in terminal differentiation, inhibition of cell proliferation, and has anti-inflammatory activities; and PPARc is involved in adipogenesis, lipid storage, and inflammation (Desvergne and Wahli, 1999; Peraza et al., 2006; Shan et al., 2008).”
Koga, T., Yao, P., Goudarzi, M., Murray, I. A., Balandaram, G., Gonzalez, F. J., Perdew, G. H., Fornace, A. J., & Peters, J. M. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.755447 · Cited by 22 · see citing works
Self-citationPPARβ/δ modulates ethanol-induced hepatic effects by decreasing pyridoxal kinase activity
Goudarzi, M., Koga, T., Khozoie, C., Mak, T. D., Kang, B.-H., Fornace, A. J., & Peters, J. M. (2013) · Toxicology · doi:10.1016/j.tox.2013.07.002 · Cited by 21 · see citing works
Self-citationComparative gene expression profiles induced by PPARγ and PPARα/γ agonists in rat hepatocytes
Rogue, A., Renaud, M. P., Claude, N., Guillouzo, A., & Spire, C. (2011) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2011.04.005 · Cited by 20 · see citing works
Chao, X., Xiong, C., Dong, W., Qu, Y., Ning, W.-D., Liu, W., Han, F., Ma, Y., Wang, R., Fei, Z., et al. (2014) · Journal of Stroke and Cerebrovascular Diseases · doi:10.1016/j.jstrokecerebrovasdis.2013.11.021 · Cited by 19 · see citing works
Pritchard, M. T., & McCracken, J. M. (2015) · Current Drug Targets · doi:10.2174/1389450116666150825111439 · Cited by 19 · see citing works
“Indeed, when MCP1 is blocked using a Spiegelmer-based inhibitor (mNOX-E36) during the resolution phase after toxic or metabolic fibrosis, further infiltration of Ly-6Chi cells is reduced favoring a shift toward the restorative Ly-6Clo subset [106]; this shift facilitates accelerated fibrosis resolution.”
BackgroundInfluentialBalandaram, G., Kramer, L. R., Kang, B.-H., Murray, I. A., Perdew, G. H., Gonzalez, F. J., & Peters, J. M. (2016) · Toxicology · doi:10.1016/j.tox.2016.07.010 · Cited by 18 · see citing works
Self-citationBalachandar, S., & Katyal, A. (2010) · European Journal of Clinical Microbiology & Infectious Diseases · doi:10.1007/s10096-010-1122-9 · Cited by 17 · see citing works
Kiani, P., Khodadadi, E. S., Nikdasti, A., Yarahmadi, S., Gheibi, M., Yousefi, Z., Ehtiati, S., Yahyazadeh, S., Shafiee, S. M., Taghizadeh, M., et al. (2025) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-025-05207-0 · Cited by 16 · see citing works
“In mice treated with a PPARβ/δ agonist (GW0742), NF-κB signaling and inflammatory signals in hepatocytes are attenuated [159].”
Wu, Q., & Liu, Q. (2012) · Hepatology Research · doi:10.1111/j.1872-034x.2012.00994.x · Cited by 14 · see citing works
PPARβ/δ: A master regulator of mesenchymal stem cell functions
Djouad, F., Ipseiz, N., Luz‐Crawford, P., Scholtysek, C., Krönke, G., & Jørgensen, C. (2016) · Biochimie · doi:10.1016/j.biochi.2016.11.011 · Cited by 13 · see citing works
Yu, Y., Wang, P. H., Cheng, W. T. K., Mersmann, H. J., Wu, S., & Ding, S. (2010) · Journal of Animal Science · doi:10.2527/jas.2009-2597 · Cited by 13 · see citing works
Peroxisome proliferator–activated receptor delta and liver diseases
Yamazaki, T., Cable, E. E., & Schnabl, B. (2025) · Hepatology Communications · doi:10.1097/hc9.0000000000000646 · Cited by 12 · see citing works
Roles of nuclear receptors in hepatic stellate cells
Pu, S., Zhou, H., Liu, Y., Liu, J., Guo, Y., & Zhou, H. (2021) · Expert Review of Gastroenterology & Hepatology · doi:10.1080/17474124.2021.1949288 · Cited by 11 · see citing works
“PPARβ duodenum, colon, large intestine [169] ↑ [39] ↑ [39] placenta, thyroid and lung [172,173] ↑ [51] n.”
BackgroundElafibranor alleviates alcohol-related liver fibrosis by restoring intestinal barrier function
Sun, Y., Wu, Y., Li, M.-R., Wei, Y.-Y., Guo, M. L., & Zhang, Z. (2024) · World Journal of Gastroenterology · doi:10.3748/wjg.v30.i43.4660 · Cited by 10 · see citing works
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“PPAR β / δ −/− mice (Shan et al., 2008 ) were kindly provided by Dr. Frank Gonzalez (NCI, NIH).”
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- Authors
- Shan, W., Palkar, P. S., Murray, I. A., McDevitt, E. I., Kennett, M. J., Kang, B. H., Isom, H. C., Perdew, G. H., Gonzalez, F. J., & Peters, J. M.
- Affiliations
- Pennsylvania State University (US)
- National Institutes of Health (US)
- Venue
- Toxicological Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-07-12
- Volume
- 105
- Issue
- 2
- Pages
- 418-428
- ISSN
- 1096-0929 (ISSN-L)
- 1096-6080
- PMC
- PMC2527639
- OpenAlex
- W2165646109
- Cited by
- 97
- References
- 101
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 11 · 2023: 4 · 2021: 6 · 2020: 7 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 11 · 2015: 3 · 2014: 2 · 2013: 5 · 2012: 7
- FWCI
- 3.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Toxicological Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA124533, CA023931, R01CA023931, R01CA124533)
- National Institute of Environmental Health Sciences (ES04869)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- PPARδ, carbon tetrachloride hepatotoxicity, GW0742, ligand activation, pro-inflammatory gene expression, TNF-α, S100A6, MCP-1, hepatic stellate cells, hepatocytes, NF-κB signaling, autocrine and paracrine signaling
- MeSH terms
- Animals, Carbon Tetrachloride, Cells, Cultured, Disease Models, Animal, Dose-Response Relationship, Drug, Ligands, Liver, Liver Diseases, Male, Mice, Inbred C57BL, Time Factors, Tumor Necrosis Factor-alpha, Biomarkers, Down-Regulation, Mice, Knockout, Inflammation Mediators, Protective Agents, PPAR delta, PPAR-beta, Cell Proliferation, Mice, Thiazolidines, Chemical and Drug Induced Liver Injury
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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