000			nab a22 7a 4500
999			_c17032 _d17032
003			PC17032
005			20221025132539.0
008			221025b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_92999 _aSanchis Gomar, Fabián _eInstituto de Investigación imas12
245	0	0	_aGalectin-3 in atrial fibrillation: Simple bystander, player or both?. _h[revisión]
260			_bClinical biochemistry, _c2015
300			_a48(12):818-22.
500			_aFormato Vancouver: Lippi G, Cervellin G, Sanchis Gomar F. Galectin-3 in atrial fibrillation: Simple bystander, player or both?. Clin Biochem. 2015 Aug;48(12):818-22.
501			_aPMID: 25952321
504			_aContiene 38 referencias
520			_aObjectives: Galectin-3 promotes fibrosis, and cardiac remodeling is a well-established cause of arrhythmias. Therefore, we reviewed current evidence on the epidemiological and biological association between galectin-3 and atrial fibrillation. Design and methods: We performed an electronic search on Medline, Scopus and Web of Science, using the keywords "galectin" OR "galectin-3" AND "atrial fibrillation" OR "arrhythmia(s)" in the fields "title/abstract/keywords". Results: Seven cohort studies were identified and reviewed. A significant association between serum galectin-3 values and the risk of atrial fibrillation was found in 4 studies (1 nested case-control, 2 case-control, 1 prospective), whereas the association could not be confirmed in a single case-control investigation. Serum galectin-3 value was also found to be a significant predictor of left atrium fibrosis, reduced left atrial volume, or decreased left ventricle ejection fraction in four studies (2 nested case-control, 2 case-control). A reliable biological explanation may be brought in support of these findings. Activated macrophages release galectin-3, which not only contributes to increase macrophages accumulation in cardiac tissue and perpetuates their activation, but also promotes fibroblast activation and proliferation, thus leading to cardiac fibrosis, cardiac remodeling, myocardiocyte dysfunction and ultimately atrial fibrillation. The onset of atrial fibrillation further amplifies macrophage activation, thus completing a vicious circle that is mirrored by evidence of substantially increased galectin-3 values in patients with persistent atrial fibrillation. Conclusions: It seems reasonable to suggest that galectin-3 measurement holds promise for stratifying risk and outcome of atrial fibrillation.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc17032.pdf _ySolicitar documento
942			_2ddc _cREV _n0