Images under the category fibrosis

  • Disruption of histamine H2 receptor slows heart failure progression through reducing myocardial apoptosis and fibrosis
    Zhi Zeng, Liang Shen, Xixian Li, Tao Luo, Xuan Wei, Jingwen Zhang, Shiping Cao, Xiaobo Huang, Yasushi Fukushima, Jianping Bin, Masafumi Kitakaze, Dingli Xu, Yulin Liao
    Clinical Science Jun 17, 2014, 127 (7) 435-448; DOI: 10.1042/CS20130716
    Figure 8
    Figure 8
    Overview of the signalling pathways of H2R activation influencing HF Pressure overload increases myocardial density of mast cells and promotes histamine production and up-regulation of H2R. Activation of H2R by histamine exerts distinct roles on fibroblasts and cardiomyocytes. In fibroblasts, H2R activation stimulates the pathway of calcineurin/nuclear translocation of NFAT/fibronectin/procollagen/cell proliferation/fibrosis, whereas in cardiomyocytes, H2R activation stimulates the pathway of mitochondrial translocation of Bax/mitochondrial permeability increase/cleavage caspase-3/apoptosis. Both fibrosis and cardiomyocyte apoptosis promote the progression of HF. αq, Gq-protein α subunit; PLC, phospholipase C; PLP2, phosphatidylinositol 4,5-bisphosphate; IP3, inositol trisphosphate; CaM, calmodulin; αs, Gs-protein α subunit.
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  • Role of Toll-like receptors in diabetic nephropathy
    Harshini Mudaliar, Carol Pollock, Usha Panchapakesan
    Clinical Science Jan 27, 2014, 126 (10) 685-694; DOI: 10.1042/CS20130267
    Figure 1
    Figure 1
    A simplified schematic diagram representing TLR2 and TLR4 signalling in the diabetic kidney The release of endogenous ligands in the diabetic milieu (hyperglycaemia, dyslipidaemia and hypoxia) activates TLR2 and TLR4 in immune and kidney cells. Activation of TLR2 initiates the MyD88-dependent pathway, whereas TLR4 engagement initiates MyD88-dependent and MyD88-independent signalling pathways. However, the pathways converge in the activation of NF-κB, which is responsible for the synthesis and secretion of pro-inflammatory cytokines, chemokines, cell adhesion molecules and pro-fibrotic markers involved in inflammation and fibrosis, eventually leading to diabetic nephropathy.
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  • Role of the TGF-β/BMP-7/Smad pathways in renal diseases
    Xiao-Ming Meng, Arthur C. K. Chung, Hui Y. Lan
    Clinical Science Oct 31, 2012, 124 (4) 243-254; DOI: 10.1042/CS20120252
    Figure 2
    Figure 2
    Therapeutic targets of TGF-β1/BMP7/Smad signalling for kidney disease (i) Administration of BMP7 attenuates renal inflammation and fibrosis. (ii) Inhibition of BMP antagonists, such as USAG-1, Gremlin, Chordin-like1, Crim1 and Kielin/Chordin-like protein (KCP), protects against renal injury; (iii) THR-123, a small-peptide agonist of BMP signalling which functions through the Alk3 receptor to inhibit renal inflammation and fibrosis. (iv) Overexpression of Smad7 suppresses NF-κB-driven renal inflammation and TGF-β/Smad3-mediated fibrosis. (v) Alteration of TGF-β/BMP-7/Smad-regulated microRNAs, such as inhibition of miR-21 and miR-192, while up-regulating miR-29 and miR-200, suppresses renal fibrosis. BMPRI etc., BMPR type I etc.; KD, knockdown; OVE, overexpression; p, phosphorylation.
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