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Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Under Re-organization)


ISSN (Print): 1871-5222
ISSN (Online): 1875-6115

Research Article

Angiotensin-II, a Potent Peptide, Participates in the Development of Hepatic Dysfunctions

Author(s): Muhammad A.T. Sagor, Muhammad M. Mohib, Muhammad S. Azam, Anisur Rahman, Foysal T. Tanmoy, Wahida K. Chowdhury, Nafees Uddin Chowdhury, Hasan M. Reza and Muhammad A. Alam*

Volume 16, Issue 3, 2016

Page: [161 - 177] Pages: 17

DOI: 10.2174/1871522217666170106103001

Price: $65


Background: Angiotensin and its precursor’s peptides contribute to multiple biological functions and regulate several important mechanisms like hormone production, fluid balance, growth, and apoptosis throughout the body. The function of Ang-II is generally mediated through AT1R and AT2R which monitor various crucial pathways. Angiotensin receptors are largely expressed in various organs such as kidney, heart, adrenal cortex, smooth muscle, brain, pancreas, endothelial cells as well as liver. Ang-II is now considered responsible for end organ dysfunction particularly mediated through oxidative stress.

Methods: We performed detailed searches in PubMed and Google scholar and compiled the literature on angiotensin mediated liver dysfunction using the key words alone or in combination such as angiotensin, liver dysfunction, oxidative stress etc.

Results: The texts and tables presented herein consolidate the current data and ongoing research regarding angiotensin II and hepatic dysfunction. A cross talk between the AT receptors, NADP(H) oxidase and mitochondrial ROS generation have been found in literatures and are now well established. These particular phenomena attributed the hepatocyte dysfunction in liver which in turn leads to hepatic inflammation and fibrosis. Hemeoxygenase, an iron metabolizing protein is also degraded by overproduction of Ang-II and AT1R that finally triggers severe hepatic injuries. Ang-II activity was also found to be increased in non-alcoholic fatty liver diseases and viral hepatitis.

Conclusion: This review work identifies the possible interaction and mechanisms of liver dysfunction mediated through Ang-II and AT receptor functions.

Keywords: Ang-II, fibrosis, free radicals, inflammation, iron overload, liver diseases.

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