Protective effect of peroxisome proliferator activated receptor gamma agonists on diabetic and non‐diabetic renal diseases

Chung, Byung Ha; Lim, Sun Woo; Ahn, Kyung Ohk; Sugawara, Akira; Ito, Sadayoshi; Choi, Bum Soon; Kim, Yong Soo; Bang, Byung Kee; Yang, Chul Woo

doi:10.1111/j.1440-1797.2005.00456.x

Cited by 39 publications

(25 citation statements)

References 55 publications

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“…In addition to their vasodilating effects on the glomerular efferent arterioles [31], their above described effects regarding lowering blood pressure as well as protecting endothelial function may possibly be involved. Additionally, reno-protective effects of PPARγ ligands in non-diabetic renal diseases have recently been reported [34], indicating the general usefulness of PPARγ ligands on chronic kidney disease. We have also demonstrated reno-protective effects of TZD rosiglitazone against cyclosporine-induced renal injury in Sprague-Dawley rats [35].…”

Section: Effects Of Pparγ On Atherosclerosismentioning

confidence: 99%

Effects of PPAR.GAMMA. on hypertension, atherosclerosis, and chronic kidney disease

et al. 2010

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Abstract. Peroxisome proliferator-activated receptor (PPAR) γ is a nuclear hormone receptor that is trans-activated by its ligands including insulin-sensitizing thiazolidinediones. PPARγ has recently been reported to demonstrate pleiotropic beneficial effects in the vasculatures, independent of its blood glucose-lowering effects. Firstly, PPARγ ligands have been shown to lower blood pressure in both animals and human. The effect may possibly be mediated via the PPARγ-mediated inhibition of the angiotensin (Ang) II type 1 receptor expression as well as Ang II-mediated signaling pathways, which may result in the suppression of the renin-angiotensin system (RAS). Secondly, the progression of atherosclerosis was also prevented by PPARγ ligands in both animals and human. In addition to the PPARγ-mediated suppression of the RAS and the thromboxane A 2 system, protective effects of PPARγ ligands on endothelial function may also be involved. Thirdly, reno-protective effects of PPARγ ligands, especially on reducing urinary albumin, have been observed in both animals and human not only in diabetic nephropathy but also in non-diabetic renal diseases. The reno-protective effects may be mediated, at least in part, via the PPARγ ligand-induced blood pressure-lowering effects, protective effects on endothelial function, and vasodilating effects on the glomerular efferent arterioles. Additionally, anti-cancer effects of PPARγ ligands have recently been reported. Taken together, usefulness and effectiveness of PPARγ ligands on lifestyle related diseases will be increasingly appreciated.

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Section: Effects Of Pparγ On Atherosclerosismentioning

confidence: 99%

Effects of PPAR.GAMMA. on hypertension, atherosclerosis, and chronic kidney disease

et al. 2010

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“…16,17). This protection reflects both improved glucose metabolism and insulin resistance as well as the antiinflammatory, antifibrotic, and antiapoptotic effects of PPARγ ligands (18).…”

Section: Role Of Ppars In Different Organs After I/r Injurymentioning

confidence: 99%

Involvement of PPAR nuclear receptors in tissue injury and wound repair

Michalik

Wahli²

2006

Journal of Clinical Investigation

203

134

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Tissue damage resulting from chemical, mechanical, and biological injury, or from interrupted blood flow and reperfusion, is often life threatening. The subsequent tissue response involves an intricate series of events including inflammation, oxidative stress, immune cell recruitment, and cell survival, proliferation, migration, and differentiation. In addition, fibrotic repair characterized by myofibroblast transdifferentiation and the deposition of ECM proteins is activated. Failure to initiate, maintain, or stop this repair program has dramatic consequences, such as cell death and associated tissue necrosis or carcinogenesis. In this sense, inflammation and oxidative stress, which are beneficial defense processes, can become harmful if they do not resolve in time. This repair program is largely based on rapid and specific changes in gene expression controlled by transcription factors that sense injury. PPARs are such factors and are activated by lipid mediators produced after wounding. Here we highlight advances in our understanding of PPAR action during tissue repair and discuss the potential for these nuclear receptors as therapeutic targets for tissue injury. An overview of tissue injuryThe clinical significance of tissue injury and the need for therapeutic agents to treat organ damage have called for an improved understanding of the causes of tissue injury and subsequent healing. The complex nature of these processes creates a challenge in identifying the specific cell types and biochemical pathways involved. Moreover, tissue protection and regeneration require tight control of cell survival and death, cell growth and differentiation, and ECM remodeling and breakdown. Chemical, biological, and mechanical stress is deleterious to epithelial tissue, and even whole organs are vulnerable to damage. For example, the liver, which metabolizes nutrients and drugs absorbed from the digestive tract, is particularly susceptible to injury, since all blood leaving the intestines and stomach must pass through it before reaching the rest of the body. Organ damage also occurs in response to an inadequate supply of oxygen (hypoxia), usually caused by blood vessel constriction or obstruction (ischemia). Under normal physiological conditions, oxygenation levels and sensitivity to hypoxia differ among the various organs. Since short periods of ischemia and reperfusion (ischemia/reperfusion, or I/R) cause extensive damage, the goal of the survival response is to maintain tissue viability. As a result, the hypoxia response requires optimal revascularization for efficient recovery.Inflammation is a major component of early healing, and its control is essential for efficient repair. The inflammatory cytokines and eicosanoids produced during the first hours after injury recruit neutrophils and macrophages to the wound. These cells amplify the early response through their production of additional inflammatory mediators. Some of these factors promote cell proliferation and migration and are thus directly involved in wound closure. ...

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“…PPAR-γ had some anti-inflammatory effects on inflammatory bowel disease and rheumatoid arthritis [30,31] . It ameliorates the inflammatory cell infiltration and downregulates the proinflammatory cytokine expression in animal models of diabetic nephropathy and lupus nephropathy as well as in mesangial cells, fibroblasts and tubular epithelial cells [32,33] . Li and colleagues demonstrated that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) could downregulate LPS-induced MCP-1 expression via the PPAR-γ pathway [34] .…”

Section: Discussionmentioning

confidence: 99%

PPAR-γ agonists inhibit TGF-β1-induced chemokine expression in human tubular epithelial cells

et al. 2008

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Protective effect of peroxisome proliferator activated receptor gamma agonists on diabetic and non‐diabetic renal diseases

Cited by 39 publications

References 55 publications

Effects of PPAR.GAMMA. on hypertension, atherosclerosis, and chronic kidney disease

Effects of PPAR.GAMMA. on hypertension, atherosclerosis, and chronic kidney disease

Involvement of PPAR nuclear receptors in tissue injury and wound repair

PPAR-γ agonists inhibit TGF-β1-induced chemokine expression in human tubular epithelial cells

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