Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-5-17
pubmed:abstractText
As a prelude to investigating the mechanism of regression of pressure overload-induced left ventricular (LV) hypertrophy (LVH), we studied the time course for the development and subsequent regression of LVH as well as accompanying alterations in cardiac function, histology, and gene expression. Mice were subjected to aortic banding for 4 or 8 wk to establish LVH, and regression was initiated by release of aortic banding for 6 wk. Progressive increase in LV mass and gradual chamber dilatation and dysfunction occurred after aortic banding. LVH was also associated with myocyte enlargement, interstitial fibrosis, and enhanced expression of atrial natriuretic peptide, collagen I, collagen III, and matrix metalloproteinase-2 but suppressed expression of alpha-myosin heavy chain and sarcoplasmic reticulum Ca(2+)-ATPase. Aortic debanding completely or partially reversed LVH, chamber dilatation and dysfunction, myocyte size, interstitial fibrosis, and gene expression pattern, each with a distinct time course. The extent of LVH regression was dependent on the duration of pressure overload, evidenced by the fact that restoration of LV structure and function was complete in animals subjected to 4 wk of aortic banding but incomplete in animals subjected to 8 wk of aortic banding. In conclusion, LVH regression comprises a variety of morphological, functional, and genetic components that show distinct time courses. A longer period of pressure overload is associated with a slower rate of LVH regression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2702-7
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:15665058-Animals, pubmed-meshheading:15665058-Atrial Natriuretic Factor, pubmed-meshheading:15665058-Calcium-Transporting ATPases, pubmed-meshheading:15665058-Collagen, pubmed-meshheading:15665058-DNA Primers, pubmed-meshheading:15665058-Disease Models, Animal, pubmed-meshheading:15665058-Echocardiography, pubmed-meshheading:15665058-Female, pubmed-meshheading:15665058-Hypertrophy, Left Ventricular, pubmed-meshheading:15665058-Male, pubmed-meshheading:15665058-Matrix Metalloproteinases, pubmed-meshheading:15665058-Mice, pubmed-meshheading:15665058-Mice, Inbred C57BL, pubmed-meshheading:15665058-Pressure, pubmed-meshheading:15665058-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15665058-Sarcoplasmic Reticulum Calcium-Transporting ATPases, pubmed-meshheading:15665058-Ventricular Pressure, pubmed-meshheading:15665058-Ventricular Remodeling
pubmed:year
2005
pubmed:articleTitle
Regression of pressure overload-induced left ventricular hypertrophy in mice.
pubmed:affiliation
Baker Heart Research Institute, PO Box 6492, St. Kilda Rd. Central, Melbourne, Victoria 8008, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't