Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endocrine glands are well vascularized and the structure of their vessels facilitates the exchange of various substances, including hormones. These glands are a frequent experimental model in research on VEGF and angiogenesis. VEGF participates in the pathogenesis of diabetes. Diabetic nephropathy is in essence a microvascular disease that develops as a result of a confluence of hemodynamic and metabolic perturbations. Diabetic retinopathy is the most common microvascular complication of diabetes mellitus and is the leading cause of blindness. In diabetic retinopathy ischemic states and hence tissue hypoxia and angiogenesis takes place. Participation of angiogenesis and VEGF in pathogenesis of neoplastic disease is described in many papers. VEGF protein and mRNA were found in cancers of the thyroid, bronchus, lungs, esophagus, stomach, colon, liver, breast, ovary, uterus, kidney, urinary bladder, in malignant tumors of the brain, bone. In a series of reports connections between the degree of VEGF expression with tumor aggressiveness and prognosis in patients have been reported. Richly vascularized are GEP NET. In neuroendocrine tumors strong expression of VEGF, Flt-1 and KDR in relation to the unchanged surrounding tissues has been demonstrated. Depending on the disease entity or the degree of its severity attempts of application the angiogenic and antiangiogenic therapy are being made. Antiangiogenic therapy (usually regarded as a form of cancer therapy) is based on: inhibitory effects of proangiogenic ligands and their receptors; stimulation or delivery of angiogenesis inhibitors; direct destruction of neoplastic tumor vasculature.
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PMID:[Vascular endothelial growth factor (VEGF) in endocrinology and oncology]. 2216 82

Given the importance of G-protein coupled receptors in the regulation of many physiological functions, deciphering the relationships between genotype and phenotype in past and present hominin GPCRs is of main interest to understand the evolutionary process that contributed to the present-day variability in human traits and health. Here, we carefully examined the publicly available genomic and protein sequence databases of the archaic hominins (Neanderthal and Denisova) to draw up the catalog of coding variations in GPCRs for peptide ligands, in comparison with living humans. We then searched in the literature the functional changes, phenotypes and risk of disease possibly associated with the detected variants. Our survey suggests that Neanderthal and Denisovan hominins were likely prone to lower risk of obesity, to enhanced platelet aggregation in response to thrombin, to better response to infection, to less anxiety and aggressiveness and to favorable sociability. While some archaic variants were likely advantageous in the past, they might be responsible for maladaptive disorders today in the context of modern life and/or specific regional distribution. For example, an archaic haplotype in the neuromedin receptor 2 is susceptible to confer risk of diabetic nephropathy in type 1 diabetes in present-day Europeans. Paying attention to the pharmacological properties of some of the archaic variants described in this study may be helpful to understand the variability of therapeutic efficacy between individuals or ethnic groups.
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PMID:The repertoire of family A-peptide GPCRs in archaic hominins. 3156 Sep 50