Since
angiotensin increases the expression of
plasminogen activator inhibitor (PAI), mechanisms associated with an actively functioning renin-angiotensin-aldosterone system can be expected to be associated with increased
PAI-1 expression. These mechanisms are present not only in common conditions resulting in glomerulosclerosis associated with aging, diabetes or genetic mutations, but also in
autoimmune disease (like scleroderma and lupus),
radiation injury,
cyclosporine toxicity, allograft nephropathy and
ureteral obstruction. While the renin-angiotensin-aldosterone system and
growth factors, such as
transforming growth factor-beta (TGF-β), are almost always part of the process, there are rare experimental observations of
PAI-1 expression without their interaction. Here we review the literature on
PAI-1 and its role in vascular, fibrotic and oxidative injury as well as work suggesting potential areas of intervention in the pathogenesis of multiple disorders.