The expression of atrial natriuretic polypeptide (ANP) in the ventricles of human hearts with myocardial infarction (MI) was studied immunohistochemically. Immunoreactive myocytes were identified in the ventricular tissues of all of 16 hearts with old MI (both with and without heart failure) and in all five hearts with subacute MI, but not in any of the eight hearts without MI nor in the five with acute MI. In the nonfailing hearts with MI, ANP positive myocytes surrounded the areas of infarction, and were also seen in the subendocardium of the infarcted segment. In the failing hearts with MI, ANP expression was noted in the whole ventricular subendocardial region, in addition to the border of infarcts. The sites of ANP expression corresponded well to those of marked stress attributable to tissue shrinkage or fibrosis due to MI, haemodynamic overload, or both. It thus appears that ANP expression is augmented in human hearts with MI regardless of the presence or absence of heart failure, and it is suggested that regional mechanical stress on the ventricular myocardium, as well as haemodynamic overload, may be very closely associated with ventricular ANP expression.
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http://dx.doi.org/10.1002/path.1711610404 | DOI Listing |
Mol Ther Nucleic Acids
March 2025
Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, China.
Preeclampsia (PE) is a significant complication of pregnancy, occurring in approximately 10% of pregnancies. However, the underlying mechanisms of this condition remain unclear. Placentation and tumorigenesis both share many characteristics, but PE is the result of insufficient placentation, in contrast to the overaggression of tumorigenesis.
View Article and Find Full Text PDFMol Biol Rep
December 2024
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Background: The role of 1,25-dihydroxyvitamin-D3 (VitD) and sirtuin-1 (SIRT1) in mitigating pathological cardiac remodeling is well recognized. However, the potential for SIRT1 to mediate the inhibitory effects of VitD on angiotensin II (Ang II) -induced hypertrophy in H9c2 cardiomyoblasts remains unclear.
Methods: H9c2 cardiomyoblasts were exposed to Ang II or a combination of VitD and Ang II, both in the absence and presence of SIRT1-specific siRNA.
Zhongguo Zhong Yao Za Zhi
October 2024
Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing Key Laboratory of Chinese Materia Pharmacology, National Clinical Research Center of Traditional Chinese Medicine for Cardiovascular Diseases Beijing 100091, China Heilongjiang University of Chinese Medicine Harbin 150040, China.
To explore the regulation of vasodilatory function in rats with post-infarction heart failure by salvianolic acid B(Sal-B) based on the mechanosensitive ion channel, namely Piezo1. A post-infarction heart failure model of rats was prepared by ligation of the left anterior descending coronary artery. After successful modeling, the rats were randomly divided into the model group, Sal-B group(0.
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View Article and Find Full Text PDFJ Cell Mol Med
December 2024
Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, Université de Lille, Lille, France.
Chronic pressure overload induces adverse cardiac remodelling characterised by left ventricular (LV) hypertrophy and fibrosis, leading to heart failure (HF). Identification of new biomarkers for adverse cardiac remodelling enables us to better understand this process and, consequently, to prevent HF. We recently identified clusterin (CLU) as a biomarker of cardiac remodelling and HF after myocardial infarction.
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