Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors describe various mechanisms (including cellular and molecular ones) that mediate the realization of interstitial inflammation under the influence of proteinuria components. The paper covers epithelial cell transdifferentiation processes, the role of angiotensin II, transforming growth factor beta, nuclear transcription factor NFkB, chemokines, endothelial factors etc. The effects of drugs routinely used in nephrology at present (angiotensin converting enzyme inhibitors, statines etc.) are presented in a new way according to the modern conception of the mechanisms of proteinuria-induced renal interstitial tissue remodeling in glomerulonephritis. The authors consider administration of antichemokine agents, which influences chemokine/chemokine receptor system, to be a prospective independent immunotherapeutic direction in treatment, aimed at prevention of glomerulonephritis progression.
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PMID:[Proteinuria-induced mechanisms of tubulointerstitial remodeling and possibilities of nephroprotection in glomerulonephritis]. 1571 47

The discovery of stem cells (SC) has shed new light on the understanding of mechanisms responsible for ischemic and degenerative disorders, and opened a new field for regenerative medicine. Furthermore, dysregulation of SC self-renewal and their transformation seem to be involved also in the development of cancer, suggesting that pharmacological treatment devoted to regulate SC genomic and phenotypic functions might represent a potential new strategy even for the treatment of neoplastic disorders. SC display a promiscuous set of transcription factors and an open chromatin structure which are required to maintain their multipotentiality, while they are progressively quenched during differentiation into specific multiple lineages. The mechanisms that govern stem cell fate decisions are under tight control but remain potentially alterable. Recent studies have shown that several currently used drugs such as colony stimulating factors, statins, angiotensin-II receptor antagonists/ACE-inhibitors, Erythropoietin, nitric oxide donors, estrogens and glitazones, have modulatory activity on SC functions. These drugs mostly enhance SC survival and mobilization. Furthermore, a series of new pharmacological agents such as the chemokine receptor antagonist AMD3100, glycogen synthase kinase-3 (GSK-3) inhibitors and histone deacetylase inhibitors (HDACi), that modulate the growth, differentiation and mobilization of SC, have been recently discovered and are currently under evaluation in both in vivo experimental models and preliminary clinical trials. Thus, modulation of SC properties through pharmacological treatment represents a new field of investigation which may lead to the development of novel strategies for the treatment not only of ischemic and degenerative disorders, but also of cancer.
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PMID:Pharmacological modulation of stem cell function. 1745 26

The study included 243 patients with acute community-acquired pneumonia and 173 healthy subjects. The following candidate loci were used to investigate genetic variability: 3 sites of CYP1A1, GSTM1, GSTT1, GSTP1, ACE gene of the rennin-angiotensin system, chemokine receptor gene CCR5. Enhanced predisposition to pneumonia was shown to be characteristic of homozygotes in deletion at the ACE locus (OR = 1.8; p = 0.013), carriers of normal alleles of the GSTM1 locus (OR = 1.7; p = 0.010), and homozygotes in allele 606T of the CYP1A1 gene (OR = 1.6; p = 0.020).
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PMID:[Genetic study of predisposition to community-acquired pneumonia]. 2231 1