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Irina N. Baranova on Muck Rack

Irina N. Baranova

As seen in: MDPI, Physiological Reports, The Journal of Immunology
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Articles

Class B Scavenger Receptor CD36 as a Potential Therapeutic Target in Inflammation Induced by Danger-Associated Molecular Patterns

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By Irina N. Baranova, Alexander V. Bocharov, Zhigang Chen, Tatyana G. Vishnyakova
| MDPI
All articles published by MDPI are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by MDPI, including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https://www.mdpi.com/openaccess.
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TLR4 mutant mice are protected from renal fibrosis and chronic kidney disease progression

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By Takayuki Tsuji, Irina N. Baranova, Alexander V. Bocharov, Kenneth J. Wilkins
| Physiological Reports Verified
AbstractChronic kidney disease (CKD) is associated with persistent low?grade inflammation and immunosuppression. In this study we tested the role of Toll?like receptor 4, the main receptor for endotoxin (LPS), in a mouse model of renal fibrosis and in a model of progressive CKD that better resembles the human disease. C3HeJ (TLR4 mutant) mice have a missense point mutation in the TLR4 gene, rendering the receptor nonfunctional.
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Synthetic Amphipathic Helical Peptides Targeting CD36 Attenuate Lipopolysaccharide-Induced Inflammation and Acute Lung Injury

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By Anna Birukova, Alexander V. Bocharov, Tinghuai Wu, Irina N. Baranova, Denis Sviridov
| The Journal of Immunology Verified
Synthetic amphipathic helical peptides (SAHPs) designed as apolipoprotein A-I mimetics are known to bind to class B scavenger receptors (SR-Bs), SR-BI, SR-BII, and CD36, receptors that mediate lipid transport and facilitate pathogen recognition. In this study, we evaluated SAHPs, selected for targeting human CD36, by their ability to attenuate LPS-induced inflammation, endothelial barrier dysfunction, and acute lung injury (ALI).
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