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Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review

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ABSTRACT

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.

No MeSH data available.


Pathologic vascular changes associated with PAI-1. LDL, low-density lipoprotein.
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SFW080F2: Pathologic vascular changes associated with PAI-1. LDL, low-density lipoprotein.

Mentions: Table 1 lists medications that have an effect on the expression of PAI-1. Most are included in the text, but several were beyond the scope of the discussion. Drugs that directly address glycemia control include insulin, which increases the expression of PAI-1. On the other hand, metformin, glipizide, troglitazone, rosiglitazone and pioglitazone are associated with decreased expression of PAI-1. Several sulfonylurea drugs (chlorpropamide, glyburide, tolazamide, tolbutamide) increase PAI-1 expression. Agents for treatment of elevated lipids lower PAI-1 expression as do ACE inhibitors, angiotensin receptor blockers and beta-blockers. Figures 1 and 2 summarize the role of PAI-1 in vascular injury and fibrosis.Fig. 1.


Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review
Pathologic vascular changes associated with PAI-1. LDL, low-density lipoprotein.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5036907&req=5

SFW080F2: Pathologic vascular changes associated with PAI-1. LDL, low-density lipoprotein.
Mentions: Table 1 lists medications that have an effect on the expression of PAI-1. Most are included in the text, but several were beyond the scope of the discussion. Drugs that directly address glycemia control include insulin, which increases the expression of PAI-1. On the other hand, metformin, glipizide, troglitazone, rosiglitazone and pioglitazone are associated with decreased expression of PAI-1. Several sulfonylurea drugs (chlorpropamide, glyburide, tolazamide, tolbutamide) increase PAI-1 expression. Agents for treatment of elevated lipids lower PAI-1 expression as do ACE inhibitors, angiotensin receptor blockers and beta-blockers. Figures 1 and 2 summarize the role of PAI-1 in vascular injury and fibrosis.Fig. 1.

View Article: PubMed Central - PubMed

ABSTRACT

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.

No MeSH data available.