ஐ.எஸ்.எஸ்.என்: 2155-9899
Harald Seeger, Stephan Segerer
Progressive kidney diseases are characterized by the recruitment of inflammatory cells to the tubulointerstitium, tubular atrophy and fibrosis. The number of lymphatic vessels increases in the interstitium during this process (i.e. neolymphangiogenesis). Here we will describe the current evidence for neolymphangiogenesis during renal injury, summarize the major factors involved and discuss the functional consequences. Data are emerging that central profibrotic players like TGF-β also mediate the release of lymphangiogenic factors such as VEGF-C and VEGF-D in the kidney. Furthermore, in other organs activation of TGF-β by VEGF-C has been described. The complex interactions of profibrotic and lymphangiogenic factors might explain why lymphangiogenesis was found to be associated with fibrosis in some models, but a reduction in fibrosis in others. It is likely that the functional consequences of lymphangiogenesis depend on the stage of the disease course and the microenvironment where it takes place. Studies are needed where lymphangiogenesis is switched on or off at defined time points. However such data are not yet available in models of renal diseases.