This report describes an investigation of the effects of developing hypertension on the synthesis and accumulation of insoluble elastin in the thoracic aorta of young rats. Uninephrectomized male rats were made hypertensive by administration of deoxycorticosterone acetate and addition of 1% NaCl to their drinking water. Divergence of systolic blood pressures between treated and control animals and hypertrophy of the vessel began after about 2 weeks of treatment. Coincident with the appearance of hypertrophy, there was an increased accumulation of insoluble elastin in the aorta and a large increase in the capacity of the aortic tissue to synthesize elastin. However, in spite of continued increases in blood pressure and vessel hypertrophy, this effect on elastin synthesis and accumulation was transient. The results of this study suggest that synthesis of elastin in aortic tissue of young rats is highly sensitive to alterations in blood pressure.
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Adv Sci (Weinh)
January 2025
Institute of Medicinal Biotechnology, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100050, P. R. China.
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January 2025
British Heart Foundation Centre for Research Excellence, School of Cardiovascular and Metabolic Medicine and Sciences, James Black Centre, King's College London, United Kingdom (C.Y.H., M.-Y.W., J.T., S.A., L.D., G.A., R.H., C.M.S.).
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View Article and Find Full Text PDFWorld J Gastroenterol
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Department of Biochemistry, School of Medicine, College of Medicine, China Medical University, Taichung 404328, Taiwan.
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View Article and Find Full Text PDFBBA Adv
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Gottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Skeletal muscle (SM) is essential for movement, stability, and overall body function, and it readily adapts to changes in energy demand. Myogenesis is energy-intensive and involves complex molecular and cellular events. We recently demonstrated that the absence of lysosomal acid lipase (LAL) significantly impacts the SM phenotype, primarily by disrupting energy homeostasis and reducing ATP production.
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