Abstract
The mesangium is a highly specialized pericapillary tissue that is involved in most pathological processes in the renal glomerulus. Three prominent proinflammatory features of intrinsic mesangial cells evolve as a result of the cross-talk with invading professional immune cells: (i) increased mediator production, (ii) increased matrix production by mesangial cells, and (iii) increased mesangial cell proliferation [1]. Resting mesangial cells do not synthesize any inflammatory mediator constitutively but require a triggering by factors secreted by professional inflammatory cells invading the glomerulus, such as macrophages or leukocytes or by factors present in serum. However, once activated, mesangial cells have the potential to become autonomous in terms of mediator production and they start to secrete a myriad of biologically active substances [1]. The orchestration of the glomerular wounding response must be exact to initiate a sophisticated orderly process of repair. The aberrant production of these mediators, however, may sustain connective tissue accumulation and result in irreversible alteration in glomerular structure and function, to end finally in what pathologists describe as glomerulosclerosis. This review focuses on a highly versatile member of this orchestra of inflammatory mediators, nitric oxide (NO), that plays a crucial role in the pathogenesis of inflammatory and autoimmune diseases.
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Pfeilschifter, J., Mühl, H. (1997). NOS in Mesangial Cells: Physiological and Pathophysiological Roles. In: Goligorsky, M.S., Gross, S.S. (eds) Nitric Oxide and the Kidney. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6039-5_10
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