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Histopathology and Doppler assessments suggested that death was due to acute congestive cardiac failure without evidence of valvular or other obvious cardiac structural abnormalities. Heart rates in Fgl2 KO embryos were significantly reduced at E8.5 and E17.5, and irregular heart rhythms were significantly more common in Fgl2 KO (21\/26) than WT (2\/21) embryos at E13.5. Indexes of systolic and\/or diastolic cardiac function were also abnormal in KO mice at E13.5 and E17.5, in postnatal mice studied at P1, and in KO mice surviving to P28. M-mode analysis showed no difference in LV diastolic chamber dimension, although posterior wall thickness was thinner at P7 and P28 in Fgl2 KO mice. We conclude that Fgl2 deficiency is not associated with obvious structural cardiac defects but is associated with a high incidence of neonatal death as well as contractile dysfunction and rhythm abnormalities during embryonic and postnatal development in mice.<\/jats:p>","DOI":"10.1152\/physiolgenomics.00026.2007","type":"journal-article","created":{"date-parts":[[2007,6,6]],"date-time":"2007-06-06T02:09:55Z","timestamp":1181095795000},"page":"53-62","source":"Crossref","is-referenced-by-count":23,"title":["<i>Fgl2<\/i>deficiency causes neonatal death and cardiac dysfunction during embryonic and postnatal development in mice"],"prefix":"10.1152","volume":"31","author":[{"given":"Junwu","family":"Mu","sequence":"first","affiliation":[{"name":"Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dawei","family":"Qu","sequence":"additional","affiliation":[{"name":"Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Agata","family":"Bartczak","sequence":"additional","affiliation":[{"name":"Multi-Organ Transplant Program, Toronto, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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