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Editorial
. 2022 Jun;33(6):1053-1055.
doi: 10.1681/ASN.2022040407.

Of Mice and MAVS-Diabetic Kidney Disease and the Leaky Gut

Ricard Farré  1 , Sander Dejongh  1   2 , Bjorn Meijers  2   3
Affiliations
Editorial

Of Mice and MAVS-Diabetic Kidney Disease and the Leaky Gut

Ricard Farré et al. J Am Soc Nephrol. 2022 Jun.
No abstract available

Keywords: diabetic nephropathy; intestine; mitochondria.

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Figures

Figure 1.
Figure 1.
The leaky gut and MAVS knockout contribute to the pathophysiology of diabetic nephropathy. (A) In normal conditions, the intestinal barrier function is intact, and luminal microbiota and endotoxins are confined to the lumen. (B) In diabetic nephropathy, deregulation of MAVS signaling in epithelial cells and the kidney alters the distribution of the microbiota and endotoxins because of (1) the presence of dysbiosis, and (2) increased paracellular, and (3) transcellular permeability. (4) Then, viable bacteria, such as Klebsiella oxytoca, can enter the systemic circulation and reach other organs, (5) including the kidney, leading to increased production of kidney injury molecule-1 (KIM-1) and renal dysfunction.
See this image and copyright information in PMC

Comment on

  • Intestinal Bacterial Translocation Contributes to Diabetic Kidney Disease.
    Linh HT, Iwata Y, Senda Y, Sakai-Takemori Y, Nakade Y, Oshima M, Nakagawa-Yoneda S, Ogura H, Sato K, Minami T, Kitajima S, Toyama T, Yamamura Y, Miyagawa T, Hara A, Shimizu M, Furuichi K, Sakai N, Yamada H, Asanuma K, Matsushima K, Wada T. Linh HT, et al. J Am Soc Nephrol. 2022 Jun;33(6):1105-1119. doi: 10.1681/ASN.2021060843. Epub 2022 Mar 9. J Am Soc Nephrol. 2022. PMID: 35264456 Free PMC article.

References

    1. Jansen J, Jansen K, Neven E, Poesen R, Othman A, van Mil A, et al. : Remote sensing and signaling in kidney proximal tubules stimulates gut microbiome-derived organic anion secretion. Proc Natl Acad Sci USA 116: 16105–16110, 2019 - PMC - PubMed
    1. Meijers B, Evenepoel P, Anders HJ: Intestinal microbiome and fitness in kidney disease. Nat Rev Nephrol 15: 531–545, 2019 - PubMed
    1. Andersen K, Kesper MS, Marschner JA, Konrad L, Ryu M, Kumar Vr S, et al. : Intestinal dysbiosis, barrier dysfunction, and bacterial translocation account for CKD-related systemic inflammation. J Am Soc Nephrol 28: 76–83, 2017 - PMC - PubMed
    1. Poesen R, Windey K, Neven E, Kuypers D, de Preter V, Augustijns P, et al. : The influence of CKD on colonic microbial metabolism. J Am Soc Nephrol 27: 1389–1399, 2016 - PMC - PubMed
    1. Joossens M, Faust K, Gryp T, Nguyen ATL, Wang J, Eloot S, et al. : Gut microbiota dynamics and uraemic toxins: One size does not fit all. Gut 68: 2257–2260, 2019 - PMC - PubMed

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