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8 in total

1. Stretch-induced programmed myocyte cell death.

Authors: W Cheng; B Li; J Kajstura; P Li; M S Wolin; E H Sonnenblick; T H Hintze; G Olivetti; P Anversa
Journal: J Clin Invest Date: 1995-11 Impact factor: 14.808

2. Myocardial cell lesions caused by an anabolic hormone.

Authors: H Behrendt; H Boffin
Journal: Cell Tissue Res Date: 1977-07-15 Impact factor: 5.249

3. Up-regulation of AT(1) and AT(2) receptors in postinfarcted hypertrophied myocytes and stretch-mediated apoptotic cell death.

Authors: A Leri; Y Liu; B Li; F Fiordaliso; A Malhotra; R Latini; J Kajstura; P Anversa
Journal: Am J Pathol Date: 2000-05 Impact factor: 4.307

4. Stretch-mediated release of angiotensin II induces myocyte apoptosis by activating p53 that enhances the local renin-angiotensin system and decreases the Bcl-2-to-Bax protein ratio in the cell.

Authors: A Leri; P P Claudio; Q Li; X Wang; K Reiss; S Wang; A Malhotra; J Kajstura; P Anversa
Journal: J Clin Invest Date: 1998-04-01 Impact factor: 14.808

5. Chronic coronary artery constriction leads to moderate myocyte loss and left ventricular dysfunction and failure in rats.

Authors: P Anversa; X Zhang; P Li; J M Capasso
Journal: J Clin Invest Date: 1992-02 Impact factor: 14.808

Ultrastructural basis of acute left ventricular failure from severe acute aortic stenosis in the rabbit.

1. Stretch-induced programmed myocyte cell death.

2. Myocardial cell lesions caused by an anabolic hormone.

3. Up-regulation of AT(1) and AT(2) receptors in postinfarcted hypertrophied myocytes and stretch-mediated apoptotic cell death.

4. Stretch-mediated release of angiotensin II induces myocyte apoptosis by activating p53 that enhances the local renin-angiotensin system and decreases the Bcl-2-to-Bax protein ratio in the cell.

5. Chronic coronary artery constriction leads to moderate myocyte loss and left ventricular dysfunction and failure in rats.

6. Histopathology of early myocardial infarcts. A new approach.

7. Insufficiency of hypertrophied heart.

8. Ex vivo stretch reveals altered mechanical properties of isolated dystrophin-deficient hearts.