The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Interactions of Transforming Growth Factor-β and Angiotensin II in Renal Fibrosis
Open accessAbstract
Overproduction of transforming growth factor-β clearly underlies tissue fibrosis in numerous experimental and human diseases. Transforming growth factor-β’s powerful fibrogenic action results from simultaneous stimulation of matrix protein synthesis, inhibition of matrix degradation, and enhanced integrin expression that facilitates matrix assembly. In animals, overexpression of transforming growth factor-β by intravenous injection, transient gene transfer, or transgene insertion has shown that the kidney is highly susceptible to rapid fibrosis. The same seems true in human disease, where excessive transforming growth factor-β has been demonstrated in glomerulonephritis, diabetic nephropathy, and hypertensive glomerular injury. A possible explanation for the kidney’s particular susceptibility to fibrosis may be the recent discovery of biologically complex interactions between the renin-angiotensin system and transforming growth factor-β. Alterations in glomerular hemodynamics can activate both the renin-angiotensin system and transforming growth factor-β. Components of the renin-angiotensin system act to further stimulate production of transforming growth factor-β and plasminogen activator inhibitor leading to rapid matrix accumulation. In volume depletion, transforming growth factor-β is released from juxtaglomerular cells and may act synergistically with angiotensin II to accentuate vasoconstriction and acute renal failure. Interaction of the renin-angiotensin system and transforming growth factor-β has important clinical implications. The protective effect of inhibition of the renin-angiotensin system in experimental and human kidney diseases correlates closely with the suppression of transforming growth factor-β production. This suggests that transforming growth factor-β, in addition to blood pressure, should be a therapeutic target. Higher doses or different combinations of drugs that block the renin-angiotensin system or entirely new drug strategies may be needed to achieve a greater antifibrotic effect.
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Cites
The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy
Lewis, E. J., Hunsicker, L. G., Bain, R. P., & Rohde, R. D. (1993) · New England Journal of Medicine · doi:10.1056/nejm199311113292004 · Cited by 5,394
Cited by
Vascular Remodeling in Hypertension: Roles of Apoptosis, Inflammation, and Fibrosis
Intengan, H. D., & Schiffrin, E. L. (2001) · Hypertension · doi:10.1161/hy09t1.096249 · Cited by 979
Angiotensin II induces contraction and proliferation of human hepatic stellate cells
Bataller, R., Ginès, P., Nicolás, J. M., Görbig, M. N., Garcia–Ramallo, E., Gasull, X., Bosch, J., Arroyo, V., & Rodés, J. (2000) · Gastroenterology · doi:10.1016/s0016-5085(00)70368-4 · Cited by 490
COVID-19 cytokine storm: the anger of inflammation
Mahmudpour, M., Roozbeh, J., Keshavarz, M., Farrokhi, S., & Nabipour, I. (2020) · Cytokine · doi:10.1016/j.cyto.2020.155151 · Cited by 461
Proinflammatory actions of angiotensins
Ruiz-Ortega, M., Lorenzo, O., Suzuki, Y., Rupérez, M., & Egido, J. (2001) · Current Opinion in Nephrology and Hypertension · doi:10.1097/00041552-200105000-00005 · Cited by 412
NOGUEIRA, A., PIRES, M. J., & OLIVEIRA, P. A. (2017) · In Vivo · doi:10.21873/invivo.11019 · Cited by 382
Metadata
- Authors
- Border, W. A., & Noble, N. A.
- Venue
- Hypertension
- Published
- 1998-01
- Volume
- 31
- Issue
- 1
- Pages
- 181-188
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2128520582
- Cited by
- 447
- References
- 1
- FWCI
- 23.25
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Border, W. A., & Noble, N. A. (1998). Interactions of Transforming Growth Factor-β and Angiotensin II in Renal Fibrosis. Hypertension. https://doi.org/10.1161/01.hyp.31.1.181
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