2003
DOI: 10.1016/s0041-1345(03)00789-9
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Extracellular matrix proteins, proteolytic enzymes, and TGF-Beta1 in the renal arterial wall of chronically rejected renal allografts

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Cited by 4 publications
(4 citation statements)
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“…In kidney and heart transplantation in the clinic, there is a strong correlation between graft-infiltrating M2 cells and signs of interstitial fibrosis, suggesting that M2 macrophages have the potential to promote development of interstitial fibrosis (5, 30, 31). Mechanistically, M2 cells can produce growth factors such as TGF-β and PDGF, which are crucial mediators of vascular changes by inducing smooth muscle cell proliferation, activation of myofibroblasts and extracellular matrix deposition (32, 33). Moreover, a recent report indicates that α-SMA + myofibroblasts contributes to interstitial fibrosis in chronic renal allograft injury, and approximately 50% of these myofibroblasts are derived from M2 macrophages (34).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In kidney and heart transplantation in the clinic, there is a strong correlation between graft-infiltrating M2 cells and signs of interstitial fibrosis, suggesting that M2 macrophages have the potential to promote development of interstitial fibrosis (5, 30, 31). Mechanistically, M2 cells can produce growth factors such as TGF-β and PDGF, which are crucial mediators of vascular changes by inducing smooth muscle cell proliferation, activation of myofibroblasts and extracellular matrix deposition (32, 33). Moreover, a recent report indicates that α-SMA + myofibroblasts contributes to interstitial fibrosis in chronic renal allograft injury, and approximately 50% of these myofibroblasts are derived from M2 macrophages (34).…”
Section: Discussionmentioning
confidence: 99%
“…5,30,31 Mechanistically, M2 cells can produce growth factors such as transforming growth factor-β and platelet-derived growth factor, which are crucial mediators of vascular changes, by inducing smooth muscle cell proliferation, activation of myofibroblasts, and extracellular matrix deposition. 32,33 Moreover, a recent report indicates that α-smooth muscle actin positive myofibroblasts contribute to interstitial fibrosis in chronic renal allograft injury, and that approximately 50% of these myofibroblasts are derived from M2 macrophages. 34 All these studies suggest the significance of M2 macrophages in mediating chronic allograft rejection.…”
Section: Data From Clinical and Preclinical Studies Repeatedly Demonsmentioning
confidence: 99%
“…In addition, cathepsin‐B can degrade fibrinogen, type IV collagen, basement membrane components and fibronectin (26). Furthermore, cathepsin‐B can activate latent collagenases, thus playing an indirect role extracellular matrix metabolism (27). Thus, we believe not only cathepsin‐L but also cathepsin‐B plays various roles in the development of cyclosporin A‐induced gingival overgrowth, since impairment of these enzymatic cascades may be initiated by cathepsin‐B suppression.…”
Section: Discussionmentioning
confidence: 99%
“…During chronic rejection, M2-like macrophages exhibit distinct functions [ 40 , 41 ], including the production of growth factors like TGF-β and PDGF. These growth factors trigger vascular changes by inducing smooth muscle cell proliferation, myofibroblast activation, and extracellular matrix deposition [ 42 , 43 ]. Furthermore, studies have shown that α-SMA + myofibroblasts contribute to interstitial fibrosis in chronic kidney transplant injury, with approximately 50 % of myofibroblasts derived from M2-like macrophages [ 44 ].…”
Section: Induce Graft Tolerance With Macrophages As Targetsmentioning
confidence: 99%