The Role of Inflammatory Cytokines in Diabetic Nephropathy

Navarro‐González, Juan F.; Mora‐Fernández, Carmen

doi:10.1681/asn.2007091048

Cited by 782 publications

(665 citation statements)

References 122 publications

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“…26,27 TNF-a and TGF-b are also critical inflammatory cytokines involved in diabetic nephropathy. 28,29 Collectively, these data indicate that the LXR agonist T0901317 inhibits diabetes-induced macrophage recruitment and inflammatory gene expression in the kidney.…”

Section: Lxr Agonist Suppresses Diabetes-induced Opn Expression In Thmentioning

confidence: 79%

Activation of Liver X Receptor Inhibits Osteopontin and Ameliorates Diabetic Nephropathy

Tachibana¹,

Ogawa

Matsushita³

et al. 2012

Journal of the American Society of Nephrology

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Osteopontin is a proinflammatory cytokine and monocyte chemoattractant implicated in the pathogenesis of diabetic nephropathy. Synthetic agonists for liver X receptors (LXRs) suppress the expression of proinflammatory genes, including osteopontin, but whether LXR activation modulates diabetic nephropathy is unknown. We administered the LXR agonist T0901317 to mice with streptozotocin-induced diabetes and evaluated its effects on diabetic nephropathy. The LXR agonist decreased urinary albumin excretion without altering blood glucose levels and substantially attenuated macrophage infiltration, mesangial matrix accumulation, and interstitial fibrosis. LXR activation suppressed the gene expression of inflammatory mediators, including osteopontin, in the kidney cortex. In vitro, LXR activation suppressed osteopontin expression in proximal tubular epithelial cells by inhibiting AP-1-dependent transcriptional activation of the osteopontin promoter. Taken together, these results suggest that inhibition of renal osteopontin by LXR agonists may have therapeutic potential for diabetic nephropathy.

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Section: Lxr Agonist Suppresses Diabetes-induced Opn Expression In Thmentioning

confidence: 79%

Activation of Liver X Receptor Inhibits Osteopontin and Ameliorates Diabetic Nephropathy

Tachibana¹,

Ogawa

Matsushita³

et al. 2012

Journal of the American Society of Nephrology

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“…[33][34][35] Proinflammatory cytokines, such as TNF-a, promote renal injury and dysfunction, which are accompanied by increased generation of reactive oxygen species. 36,37 In this regard, antiinflammatory agents have been reported to attenuate the progression of kidney damage. [38][39][40] Our study with loss-of-function genetic manipulations indicates that reduced levels of circulating Fstl1 exacerbate renal injury after subtotal nephrectomy, with an accompanying upregulation of proinflammatory cytokines and NADPH oxidase components that are the major source of reactive oxygen species.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Hayakawa¹,

Ohashi

Shibata³

et al. 2015

Journal of the American Society of Nephrology

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Heart disease contributes to the progression of CKD. Heart tissue produces a number of secreted proteins, also known as cardiokines, which participate in intercellular and intertissue communication. We recently reported that follistatin-like 1 (Fstl1) functions as a cardiokine with cardioprotective properties. Here, we investigated the role of cardiac Fstl1 in renal injury after subtotal nephrectomy. Cardiac-specific Fstl1-deficient (cFstl1-KO) mice and wild-type mice were subjected to subtotal (5/6) nephrectomy. cFstl1-KO mice showed exacerbation of urinary albumin excretion, glomerular hypertrophy, and tubulointerstitial fibrosis after subtotal renal ablation compared with wild-type mice. cFstl1-KO mice also exhibited increased mRNA levels of proinflammatory cytokines, including TNF-a and IL-6, NADPH oxidase components, and fibrotic mediators, in the remnant kidney. Conversely, systemic administration of adenoviral vectors expressing Fstl1 (Ad-Fstl1) to wild-type mice with subtotal nephrectomy led to amelioration of albuminuria, glomerular hypertrophy, and tubulointerstitial fibrosis, accompanied by reduced expression of proinflammatory mediators, NADPH oxidase components, and fibrotic markers in the remnant kidney. In cultured human mesangial cells, treatment with recombinant FSTL1 attenuated TNF-a-stimulated expression of proinflammatory cytokines. Treatment of mesangial cells with FSTL1 augmented the phosphorylation of AMP-activated protein kinase (AMPK), and inhibition of AMPK activation abrogated the anti-inflammatory effects of FSTL1. These data suggest that Fstl1 functions in cardiorenal communication and that the lack of Fstl1 production by myocytes promotes glomerular and tubulointerstitial damage in the kidney.

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“…Moreover, TNF-α can increase the release of other cytokines, chemokines, growth factors, and acute phase proteins [30,31]. As a pleiotropic cytokine, TNF-α exerts multiple effects and it can contribute to the development of diabetic nephropathy through several mechanisms [30].…”

Section: Discussionmentioning

confidence: 99%

Apelin activates the expression of inflammatory cytokines in microglial BV2 cells via PI-3K/Akt and MEK/Erk pathways

Chen

Tao

Jiang

2015

Sci. China Life Sci.

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The Role of Inflammatory Cytokines in Diabetic Nephropathy

Cited by 782 publications

References 122 publications

Activation of Liver X Receptor Inhibits Osteopontin and Ameliorates Diabetic Nephropathy

Activation of Liver X Receptor Inhibits Osteopontin and Ameliorates Diabetic Nephropathy

Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Apelin activates the expression of inflammatory cytokines in microglial BV2 cells via PI-3K/Akt and MEK/Erk pathways

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