{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T12:30:44Z","timestamp":1792758644328,"version":"4.5.0"},"reference-count":46,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2019,11,6]],"date-time":"2019-11-06T00:00:00Z","timestamp":1572998400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2020,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>Dilated cardiomyopathy (DCM) is characterised by left ventricular dilation and associated with systolic dysfunction. Recent evidence has reported the high expression of latent transforming growth factor beta binding protein 2 (LTBP2) in heart diseases, which may play a role in regulating multiple biological functions of myocardial cells. Thus, this study set out to investigate the molecular mechanism and effects of LTBP2 in myocardial oxidative stress injury, fibrosis and remodelling in a rat model of DCM, with the involvement of NF\u2010\u03baB signalling pathway.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The rat model of DCM was treated with si\u2010LTBP2 and\/or activator of NF\u2010\u03baB signalling pathway to examine the haemodynamic indexes, cardiac functions, oxidative stress injury, fibrosis and remodelling. Moreover, in vitro experiments were conducted to verify the regulatory role of LTBP2 and NF\u2010\u03baB signalling pathway in DCM.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>LTBP2 was up\u2010regulated in DCM rats. After LTBP2 was knocked down, haemodynamic indexes, HW\/BW ratio, collagen volume fraction (CVF) level, positive expression of LTBP2, levels of reactive oxygen species (ROS), malondialdehyde (MDA), interleukin\u20106 (IL\u20106), tumour necrosis factor\u2010alpha (TNF\u2010\u03b1), tumour necrosis factor beta 1 (TGF\u2010\u03b21) and brain natriuretic peptide (BNP) were all decreased. Meanwhile, levels of LTBP2, Col\u2010I, Col\u2010III, p65 and p52 were also reduced, while HW, BW and levels of SOD and TAOC were increased. In contrast, activation of NF\u2010\u03baB signalling pathway reversed effects of LTBP2 gene silencing. These findings were confirmed by in vivo experiments.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>LTBP2 silencing can attenuate myocardial oxidative stress injury, myocardial fibrosis and myocardial remodelling in DCM rats by down\u2010regulating the NF\u2010\u03baB signalling pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.13377","type":"journal-article","created":{"date-parts":[[2019,9,12]],"date-time":"2019-09-12T02:13:22Z","timestamp":1568254402000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["LTBP2 knockdown by siRNA reverses myocardial oxidative stress injury, fibrosis and remodelling during dilated cardiomyopathy"],"prefix":"10.1111","volume":"228","author":[{"given":"Xue\u2010Feng","family":"Pang","sequence":"first","affiliation":[{"name":"Department of 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