Regular ArticleCultured Myofibroblasts Generate Angiotensin Peptidesde Novo
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RAS inhibition in resident fibroblast biology
2021, Cellular SignallingCitation Excerpt :All the necessary components for the generation of Ang II can be found in the left ventricle (LV) [14,15]. Moreover, cardiac fibroblasts also express genes for renin, ACE, angiotensinogen, as well as the AT1 and AT2 receptors [4,16–21]. Ang II also stimulates aldosterone release from the adrenal cortex, which promotes fibrosis in the heart via the mineralocorticoid receptor.
Pro-remodeling peptides modulate collagen α1(I) promoter activity in rat cardiac myofibroblasts
2019, Biochemical and Biophysical Research CommunicationsWhat is the role of peptide fragments of collagen I and IV in health and disease?
2019, Life SciencesCitation Excerpt :There is constant turnover of collagen throughout the human body, especially within the interstitial matrix of tissues. It has been known for over a decade now that myofibroblasts of cardiac connective tissue are local sources of peptides such as angiotensin and endothelin [7,8]. These same peptides are known to stimulate the accumulation of collagen types I and III in the cardiac interstitial matrix via fibroblast and myofibroblast cells, with endothelin-1 even reducing collagenase activity [9].
SIRT3-mediated cardiac remodeling/repair following myocardial infarction
2018, Biomedicine and PharmacotherapyPersistent phenotypic shift in cardiac fibroblasts: Impact of transient renin angiotensin system inhibition
2016, Journal of Molecular and Cellular CardiologyRenal denervation has blood pressure-independent protective effects on kidney and heart in a rat model of chronic kidney disease
2015, Kidney InternationalCitation Excerpt :Unilateral renal sympathetic denervation with suppression of ipsilateral afferent signals stimulates contralateral renal efferent signals.54 With regard to AGT/AII generation in cardiac tissue, cardiac myocytes,47 fibroblasts,48 myofibroblasts,56 and monocyte/macrophages57,58 have the potential to generate AGT. In the current study, increases in cardiac AGT could be attributed to cardiac fibroblasts and macrophages.
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Please address all correspondence to: Laxmansa C. Katwa, University of Missouri Health Sciences Center, Division of Cardiology, Rm. MA432 Medical Sciences Building, Columbia, MO 65212, USA.