Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic ketoacidosis (DKA) is life-threatening acute metabolic complication of diabetes mellitus (DM) that is characterized by acidosis, ketosis, and hyperglycemia, currently affecting mostly patients under 30 years of age with diabetes mellitus type 1. In both, DM and DKA, a pro-inflammatory state exists. This clinical entity occurs as a result of hyperglycemia-induced disturbances, resulting in an increased oxidative metabolism. For the latter reason, the use of vitamin C seems promising in DKA due to its antioxidant role in reducing the superoxide radicals that are consequence of the oxidative stress. This can decrease the pro-inflammatory state and avoids complications. Vitamin C, or also known as ascorbic acid, has been widely used in several illnesses, such as common cold, tissue healing, fertility, atherosclerosis, cancer prevention, immunity restoration, neuro-degenerative disease and also has been suggested to decrease the risk of DM, and this reason is giving place to believe that vitamin C can have an important role in treating diabetic complications such as DKA. In order to counteract these oxidative disturbances in DKA patients, we analyzed the current data regarding vitamin C and evaluate its role in any type treatment of this complication in the near future.
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PMID:Role of vitamin C in diabetic ketoacidosis: Is it ready for prime time? 3058 81

Vascular calcification is a pathophysiological process that is associated with coronary atherosclerosis, and is a prognostic marker of cardiovascular morbidity and mortality. The process of arterial wall calcification is triggered and accompanied by pro-osteogenic phenotypical modifications of resident smooth muscle cells (SMC). Vitamin C (ascorbic acid) is an essential nutrient required to support the production of extracellular matrix components and maintain healthy connective tissue. In this study we investigated the effects of ascorbic acid on cultured human aortic SMC calcification process in vitro. Our results demonstrate that supplementation of SMC cultures with ascorbic acid significantly decreases calcium accumulation in SMC-produced and -deposited extracellular matrix. These effects were accompanied by a reduction in cell-associated alkaline phosphatase activity. Significantly, treatment of cultured SMC with HMG-CoA reductase inhibitors, simvastatin and mevastatin, resulted in increased calcium accumulation in cultured SMC. These effects were blocked by ascorbic acid. The effects of ascorbic acid supplementation on pro-osteogenic modification were compared in different cell types. Analysis of the expression of osteogenic markers in cultured human aortic SMC, human dermal fibroblasts and immortalized human osteoblasts (hFOB) revealed cell type-specific responses to ascorbate supplementation. We conclude that ascorbic acid supplementation can actively and beneficially interfere with the process of arterial wall calcification, with potential implications for human health.
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PMID:Vitamin C inhibits the calcification process in human vascular smooth muscle cells. 3268 68


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