2017
DOI: 10.1007/s00109-017-1540-6
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Regulation of endogenous brakes to kidney fibrosis: turning the view upside down

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Cited by 2 publications
(2 citation statements)
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“…Chronic kidney disease induces intestinal dysbiosis, which contributes to systemic inflammation (via the production of uremic toxins) thereby promoting NAFLD. Inflammation also drives renal fibrosis, which further reduces kidney function, in so doing enhances the levels of uremic toxins within the blood, creating a self-perpetuating multiorgan disease [ 189 ]. Several pro-inflammatory cytokines as well as bacterial toxins, e.g.…”
Section: Developing Topics In the Cold Shock Protein Fieldmentioning
confidence: 99%
“…Chronic kidney disease induces intestinal dysbiosis, which contributes to systemic inflammation (via the production of uremic toxins) thereby promoting NAFLD. Inflammation also drives renal fibrosis, which further reduces kidney function, in so doing enhances the levels of uremic toxins within the blood, creating a self-perpetuating multiorgan disease [ 189 ]. Several pro-inflammatory cytokines as well as bacterial toxins, e.g.…”
Section: Developing Topics In the Cold Shock Protein Fieldmentioning
confidence: 99%
“…The final common pathological manifestation of CKD is renal fibrosis in which multiple serum cytokines are involved. Given the role of renal fibrosis, Lindquist J et al proposed the novel idea that the risk for organ fibrosis should be quantifiable, similar to autoimmune disorders (autoantibody titres) or cancers (tumour markers), and that treatment options may be adjustable [32], which may decrease the mortality of CKD.…”
Section: Yb-1 and Ckdmentioning
confidence: 99%