Pubmed-entry ::= {
  pmid 22389386,
  medent {
    em std {
      year 2012,
      month 5,
      day 3
    },
    cit {
      title {
        name "Heart angiotensin II-induced cardiomyocyte hypertrophy
 suppresses coronary angiogenesis and progresses diabetic cardiomyopathy."
      },
      authors {
        names ml {
          "Masuda T",
          "Muto S",
          "Fujisawa G",
          "Iwazu Y",
          "Kimura M",
          "Kobayashi T",
          "Nonaka-Sarukawa M",
          "Sasaki N",
          "Watanabe Y",
          "Shinohara M",
          "Murakami T",
          "Shimada K",
          "Kobayashi E",
          "Kusano E"
        },
        affil str "Divisions of Nephrology and."
      },
      from journal {
        title {
          iso-jta "Am. J. Physiol. Heart Circ. Physiol.",
          ml-jta "Am J Physiol Heart Circ Physiol",
          issn "1522-1539",
          name "American journal of physiology. Heart and circulatory
 physiology"
        },
        imp {
          date std {
            year 2012,
            month 5
          },
          volume "302",
          issue "9",
          pages "H1871-H1883",
          language "eng",
          pubstatus ppublish,
          history {
            {
              pubstatus aheadofprint,
              date std {
                year 2012,
                month 3,
                day 2
              }
            },
            {
              pubstatus other,
              date std {
                year 2012,
                month 3,
                day 6,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus pubmed,
              date std {
                year 2012,
                month 3,
                day 6,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus medline,
              date std {
                year 2012,
                month 3,
                day 6,
                hour 6,
                minute 0
              }
            }
          }
        }
      },
      ids {
        pii "ajpheart.00663.2011",
        doi "10.1152/ajpheart.00663.2011",
        pubmed 22389386
      }
    },
    abstract "To examine whether and how heart ANG II influences the
 coordination between cardiomyocyte hypertrophy and coronary angiogenesis and
 contributes to the pathogenesis of diabetic cardiomyopathy, we used
 Spontaneously Diabetic Torii (SDT) rats treated without and with olmesartan
 medoxomil (an ANG II receptor blocker). In SDT rats, left ventricular (LV)
 ANG II, but not circulating ANG II, increased at 8 and 16 wk after diabetes
 onset. SDT rats developed LV hypertrophy and diastolic dysfunction at 8 wk,
 followed by LV systolic dysfunction at 16 wk, without hypertension. The SDT
 rat LV exhibited cardiomyocyte hypertrophy and increased hypoxia-inducible
 factor-1alpha expression at 8 wk and to a greater degree at 16 wk and
 interstitial fibrosis at 16 wk only. In SDT rats, coronary angiogenesis
 increased with enhanced capillary proliferation and upregulation of the
 angiogenic factor VEGF at 8 wk but decreased VEGF with enhanced capillary
 apoptosis and suppressed capillary proliferation despite the upregulation of
 VEGF at 16 wk. In SDT rats, the phosphorylation of VEGF receptor-2 increased
 at 8 wk alone, whereas the expression of the antiangiogenic factor
 thrombospondin-1 increased at 16 wk alone. All these events, except for
 hyperglycemia or blood pressure, were reversed by olmesartan medoxomil. These
 results suggest that LV ANG II in SDT rats at 8 and 16 wk induces
 cardiomyocyte hypertrophy without affecting hyperglycemia or blood pressure,
 which promotes and suppresses coronary angiogenesis, respectively, via VEGF
 and thrombospondin-1 produced from hypertrophied cardiomyocytes under chronic
 hypoxia. Thrombospondin-1 may play an important role in the progression of
 diabetic cardiomyopathy in this model.",
    pmid 22389386,
    pub-type {
      "Journal Article"
    },
    status premedline
  }
}

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