Ma, Jin J. Chadban, Steven Y. Zhao, Cathy Chen, Xiaochen Kwan, Tony Panchapakesan, Usha Pollock, Carol A. Wu, Huiling TLR4 deficiency protected diabetic kidneys from interstitial fibrosis and tubular injury. <p>(A) Significant interstitial collagen accumulation was evident in WT but not TLR4<sup>−/−</sup> mice with diabetes at 12 and 24 weeks. (B) Illustration of representative sections of the histological changes on PSR staining for collagen. (C) Immunohistochemical staining showed upregulation of α-SMA in WT, but not TLR4<sup>−/−</sup> mice, with diabetes as compared to non-diabetic controls at week 24. (D) Significant upregulation of KIM-1 was apparent in WT mice with diabetes, but attenuated in TLR4<sup>−/−</sup> diabetic kidneys. The data are present as the means ± SEM; * <i>p</i><0.05; ** <i>p</i><0.01; *** <i>p</i><0.001. The number of animals per group was described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097985#pone-0097985-g001" target="_blank">Figure 1</a>.</p> cell biology;Signal transduction;cell signaling;Membrane receptor signaling;Immune receptor signaling;Immunological signaling;Molecular cell biology;Metabolic disorders;Diabetes mellitus;Type 1 diabetes;type 2 diabetes;Nephrology;Chronic kidney disease;Model organisms;Animal models;Mouse models;deficiency;protected;diabetic;kidneys;interstitial;fibrosis;tubular 2014-05-19
    https://plos.figshare.com/articles/figure/_TLR4_deficiency_protected_diabetic_kidneys_from_interstitial_fibrosis_and_tubular_injury_/1031190
10.1371/journal.pone.0097985.g005