Endothelin-1 Increases Collagen Accumulation in Renal Mesangial Cells by Stimulating a Chemokine and Cytokine Autocrine Signaling Loop

Simonson, Michael S.; Ismail‐Beigi, Faramarz

doi:10.1074/jbc.m110.190793

Cited by 64 publications

(45 citation statements)

References 40 publications

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“…In the case of interstitial nephritis, the TECs and macrophages secrete MCP-1 (15,17,18), and MCP-1 is bound and internalized by macrophages that are chemotactically attracted to MCP-1. Accordingly, the MCP-1 equation is given by…”

Section: Equation For Tec Density (E)mentioning

confidence: 99%

“…Similarly, soluble proinflammmatory factors could "leak" out of damaged glomeruli and activate tubular epithelial cells (TECs) (11)(12)(13)(14). Activated TECs secrete a number of proinflammatory mediators including chemoattractants such as monocyte chemotactic protein-1 (MCP-1) that recruit additional circulating monocytes to the tubulointerstitial space (15)(16)(17)(18). Infiltrating monoctyes become activated macrophages and along with activated TECs perpetuate and enhance tubulointerstitial inflammation and facilitate the progression from inflammation to interstitial fibrosis by secreting a number of cytokines and growth factors (Fig.…”

mentioning

confidence: 99%

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Mathematical model of renal interstitial fibrosis

Hao¹,

Rovin²,

Friedman

2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance This paper deals with fibrosis of the kidney, a disease caused by inflammation, and so far there has been no way to diagnose and monitor the disease’s progression with noninvasive methods (the only way to determine the disease state is by biopsy, which cannot be frequently repeated). For this reason we developed a mathematical model of progression of renal fibrosis and validated it with biomarkers that were obtained from patients’ urine samples. We then used the model to show how antifibrosis drugs that are currently being developed for nonrenal fibrosis can be used to treat renal fibrosis.

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Section: Equation For Tec Density (E)mentioning

confidence: 99%

mentioning

confidence: 99%

Mathematical model of renal interstitial fibrosis

Hao¹,

Rovin²,

Friedman

2014

Proc. Natl. Acad. Sci. U.S.A.

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“…Via the AT1 receptor, angiotensin II also stimulates IL-6 production by vascular smooth muscle cells (Funakoshi et al, 1999). This pro-inflammatory effect of Ang II could thus be related to hypertension (Harrison et al, 2012) and could promote mesangial cell activation, leading to increases in the mesangial extracellular matrix (Simonson and Ismail-Beigi, 2011). Adhesion molecules expressed on cell surfaces mediate specific cell-cell interactions in embryogenesis, histogenesis, immune responses, and inflammatory reactions (Galkina and Ley, 2007).…”

Section: Discussionmentioning

confidence: 99%

Pro-inflammatory role of angiotensin II in mercuric chloride-induced nephropathy in rats

Peña

Hernández-Fonseca

Rincón

et al. 2012

Journal of Immunotoxicology

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“…There is emerging evidence of role of endothelin in the pathogenesis of proteinuria [39,40]. In addition to this, endothelin also plays a role in the upregulation of inflammation and fibrosis in renal parenchyma [41]. Therefore, endothelin antagonists were hypothesized to improve albuminuria in addition to causing anti-inflammatory and anti-fibrotic effects.…”

Section: Therapiesmentioning

confidence: 99%

Diabetic nephropathy: newer therapeutic perspectives

Keri

Samji

Blumenthal

2018

Journal of Community Hospital Internal Medicine Perspectives

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Diabetic nephropathy (DN is a dreaded consequence of diabetes mellitus, accounting for about 40% of end-stage renal disease (ESRD). It is responsible for significant morbidity and mortality, both directly by causing ESRD and indirectly by increasing cardiovascular risk. Extensive research in this field has thrown light on multiple pathways that can be pharmacologically targeted, to control or reverse the process of DN. Glomerulocentric approach of DN still continues to produce favourable results as evidenced by the recent data on SGLT-2 (sodium glucose co-transporter type 2) inhibitors. Beyond the glomerular mechanisms, numerous novel pathways have been discovered in the last decade. Some of these pathways target inflammatory and oxidative damage, while the others target more specific mechanisms such as AGE-RAGE (advanced glycation end products-receptors for advanced glycation end products), ASK (apoptotic signal-regulating kinase), and endothelin-associated pathways. As a result of the research, a handful of clinically relevant drugs have made it to the human trials which have been elucidated in the following review, bearing in the mind that there are many more to come over the next few years. Ongoing research is expected to inform the clinicians regarding the use of the newer drugs in DN.Abbreviations: USFDA: Unites States Food and Drug Administration; SGLT-2: Sodium glucose transporter type 2; GLP-1: Glucagon-like peptide-1; DDP-4: Dipeptidyl peptidase-4; UACR: urinary albumin creatinine ratio; eGFR: Estimated glomerular filtration rate; CKD: Chronic kidney disease; DN: Diabetic nephropathy; TGF: Tubuloglomerular feedback; RAAS: Renin angiotensin aldosterone system; T1DM: Type 1 diabetes mellitus; T2DM: Type 2 diabetes mellitus; RCT: Randomized controlled trial; AGE-RAGE: Advanced glycation end products-receptors for advanced glycation end products; ASK-1: Apoptotic signal-regulating kinase-1; Nrf-2: Nuclear 1 factor [erythroid derived-2]-related factor 2; ml/min/1.73m2: Millilitre/minute/1.73 square meters of body surface area; ~: Approximately.

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Endothelin-1 Increases Collagen Accumulation in Renal Mesangial Cells by Stimulating a Chemokine and Cytokine Autocrine Signaling Loop

Cited by 64 publications

References 40 publications

Mathematical model of renal interstitial fibrosis

Mathematical model of renal interstitial fibrosis

Pro-inflammatory role of angiotensin II in mercuric chloride-induced nephropathy in rats

Diabetic nephropathy: newer therapeutic perspectives

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