| pubmed-article:16646590 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16646590 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:16646590 | lifeskim:mentions | umls-concept:C0004238 | lld:lifeskim |
| pubmed-article:16646590 | lifeskim:mentions | umls-concept:C0110611 | lld:lifeskim |
| pubmed-article:16646590 | pubmed:dateCreated | 2006-5-1 | lld:pubmed |
| pubmed-article:16646590 | pubmed:abstractText | Atrial fibrillation (AF) is the most common arrhythmia in humans. AF is accompanied by a remodeling process which changes the electrophysiology of the cells and the gap junctional communication within the tissue. Gap junctions, forming communicating channels between neighboring cells, and their specific geometric arrangement seem to contribute to the initiation of AF within the pulmonary veins as well as to the stabilization of AF providing a heterogeneous biophysical network of cells enabling multiple wavelets. These tissue changes are accompanied by fibrosis and changes in the expression levels of Cx43 and Cx40, probably depending on the underlying diseases or the animal model used. New studies point to a modulating role of angiotensin II in this process and a possible therapeutic role for ACE inhibitors or AT(1) antagonists. | lld:pubmed |
| pubmed-article:16646590 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16646590 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16646590 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16646590 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16646590 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16646590 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16646590 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16646590 | pubmed:issn | 0065-2326 | lld:pubmed |
| pubmed-article:16646590 | pubmed:author | pubmed-author:DheinStefanS | lld:pubmed |
| pubmed-article:16646590 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16646590 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:16646590 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16646590 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16646590 | pubmed:pagination | 161-74 | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:meshHeading | pubmed-meshheading:16646590... | lld:pubmed |
| pubmed-article:16646590 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16646590 | pubmed:articleTitle | Role of connexins in atrial fibrillation. | lld:pubmed |
| pubmed-article:16646590 | pubmed:affiliation | Klinik für Herzchirurgie, Herzzentrum, Universität Leipzig, Leipzig, Germany. dhes@medizin.uni-leipzig.de | lld:pubmed |
| pubmed-article:16646590 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16646590 | pubmed:publicationType | Review | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16646590 | lld:pubmed |
