{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T19:24:18Z","timestamp":1791055458984,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,3,7]],"date-time":"2007-03-07T00:00:00Z","timestamp":1173225600000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2007,3]]},"abstract":"<jats:p>It is unclear whether cardiac hypertrophy and hypertrophy\u2010related pathways will be induced by long\u2010term intermittent hypoxia. Thirty\u2010six Sprague\u2013Dawley rats were randomly assigned into three groups: normoxia, and long\u2010term intermittent hypoxia (12% O<jats:sub>2<\/jats:sub>, 8 h per day) for 4 weeks (4WLTIH) or for 8 weeks (8WLTIH). Myocardial morphology, trophic factors and signalling pathways in the three groups were determined by heart weight index, histological analysis, Western blotting and reverse transcriptase\u2010polymerase chain reaction from the excised left ventricle. The ratio of whole heart weight to body weight, the ratio of left ventricular weight to body weight, the gross vertical cross\u2010section of the heart and myocardial morphological changes were increased in the 4WLTIH group and were further augmented in the 8WLTIH group. In the 4WLTIH group, tumour necrosis factor\u2010\u03b1(TNF\u03b1), insulin\u2010like growth factor (IGF)\u2010II, phosphorylated p38 mitogen\u2010activated protein kinase (P38), signal transducers and activators of transcription (STAT)\u20101 and STAT\u20103 were significantly increased in the cardiac tissues. However, in the 8WLTIH group, in addition to the above factors, interleukin\u20106, mitogen\u2010activated protein kinase (MEK)5 and extracellular signal\u2010regulated kinase (ERK)5 were significantly increased compared with the normoxia group. We conclude that cardiac hypertrophy associated with TNF\u03b1 and IGF\u2010II was induced by intermittent hypoxia. The longer duration of intermittent hypoxia further activated the eccentric hypertrophy\u2010related pathway, as well as the interleukin 6\u2010related MEK5\u2013ERK5 and STAT\u20103 pathways, which could result in the development of cardiac dilatation and pathology.<\/jats:p>","DOI":"10.1113\/expphysiol.2006.036590","type":"journal-article","created":{"date-parts":[[2006,12,22]],"date-time":"2006-12-22T01:28:53Z","timestamp":1166750933000},"page":"409-416","source":"Crossref","is-referenced-by-count":55,"title":["Eccentric cardiac hypertrophy was induced by long\u2010term intermittent hypoxia in 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