pubmed-article:18827908 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18827908 | lifeskim:mentions | umls-concept:C0016059 | lld:lifeskim |
pubmed-article:18827908 | lifeskim:mentions | umls-concept:C1524119 | lld:lifeskim |
pubmed-article:18827908 | lifeskim:mentions | umls-concept:C0342257 | lld:lifeskim |
pubmed-article:18827908 | lifeskim:mentions | umls-concept:C0175630 | lld:lifeskim |
pubmed-article:18827908 | lifeskim:mentions | umls-concept:C2745888 | lld:lifeskim |
pubmed-article:18827908 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
pubmed-article:18827908 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:18827908 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:18827908 | pubmed:dateCreated | 2008-10-1 | lld:pubmed |
pubmed-article:18827908 | pubmed:abstractText | Diabetes mellitus is characterized by a lack of insulin causing elevated blood glucose, often with associated insulin resistance. Over time, especially in genetically susceptible individuals, such chronic hyperglycemia can cause tissue injury. One pathological response to tissue injury is the development of fibrosis, which involves predominant extracellular matrix (ECM) accumulation. The main factors that regulate ECM in diabetes are thought to be pro-sclerotic cytokines and protease/anti-protease systems. This review will examine the key markers and regulators of tissue fibrosis in diabetes and whether their levels in biological fluids may have clinical utility. | lld:pubmed |
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