Andrey Kazakov
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Explore the profile of Andrey Kazakov including associated specialties, affiliations and a list of published articles.
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28
Citations
681
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Recent Articles
1.
Bettink S, Reil J, Kazakov A, Korbel C, Millenaar D, Laufs U, et al.
Biomedicines
. 2022 Oct;
10(10).
PMID: 36289897
Pressure-overload-induced cardiac hypertrophy represents one cause of the development of heart failure. The aim of this study is to characterize the influence of the TIR-domain-containing adapter-inducing interferon-β (TRIF) during afterload-induced...
2.
Wollenhaupt J, Frisch J, Harlacher E, Wong D, Jin H, Schulte C, et al.
Redox Biol
. 2022 Sep;
56:102459.
PMID: 36099852
Aims: Patients with chronic kidney disease (CKD) have an increased risk of cardiovascular events and exhibit myocardial changes including left ventricular (LV) hypertrophy and fibrosis, overall referred to as 'uremic...
3.
Selejan S, Linz D, Mauz M, Hohl M, Huynh A, Speer T, et al.
Basic Res Cardiol
. 2022 Jul;
117(1):36.
PMID: 35834066
Atrial fibrillation (AF) is highly prevalent in hypertensive patients with metabolic syndrome and is related to inflammation and activation of the sympathoadrenergic system. The multi-ligand Receptor-for-Advanced-Glycation-End-products (RAGE) activates inflammation-associated tissue...
4.
Hohl M, Selejan S, Wintrich J, Lehnert U, Speer T, Schneider C, et al.
Circ Res
. 2022 Feb;
130(6):814-828.
PMID: 35130718
Background: In patients with chronic kidney disease (CKD), atrial fibrillation (AF) is highly prevalent and represents a major risk factor for stroke and death. CKD is associated with atrial proarrhythmic...
5.
Bertero E, Nickel A, Kohlhaas M, Hohl M, Sequeira V, Brune C, et al.
Circulation
. 2021 Oct;
144(21):1694-1713.
PMID: 34648376
Background: Barth syndrome (BTHS) is caused by mutations of the gene encoding tafazzin, which catalyzes maturation of mitochondrial cardiolipin and often manifests with systolic dysfunction during early infancy. Beyond the...
6.
Kazakov A, Hall R, Werner C, Meier T, Trouvain A, Rodionycheva S, et al.
Basic Res Cardiol
. 2018 Sep;
113(6):42.
PMID: 30191336
Fibrosis is a hallmark of maladaptive cardiac remodelling. Here we report that genome-wide quantitative trait locus (QTL) analyses in recombinant inbred mouse lines of C57BL/6 J and DBA2/J strains identified...
7.
Selejan S, Linz D, Tatu A, Hohl M, Speer T, Ewen S, et al.
J Mol Cell Cardiol
. 2018 Aug;
122:34-46.
PMID: 30096408
Receptors-for-Advanced-Glycation-End-products (RAGE) activate pro-inflammatory programs mediated by carboxymethyllysine (CML) and high-mobility-group-box1 protein (HMGB1). The soluble isoform sRAGE neutralizes RAGE-ligands preventing cardiovascular complications in conditions associated with increased sympathetic activation like...
8.
Petersen J, Kazakov A, Bohm M, Schafers H, Laufs U, Abdul-Khaliq H
J Transl Med
. 2018 Apr;
16(1):111.
PMID: 29703225
Background: The aim of this study was to characterize the influence of cardiopulmonary bypass (CPB) on myocardial remodeling in newborns and children. Methods: Biopsies from the right atrium were taken...
9.
Selejan S, Hewera L, Hohl M, Kazakov A, Ewen S, Kindermann I, et al.
Shock
. 2017 Jun;
48(1):18-28.
PMID: 28608784
Background: Receptor for advanced glycation end products (RAGE) and its cleavage fragment soluble RAGE (sRAGE) are opposite players in inflammation. Enhanced monocytic RAGE expression and decreased plasma sRAGE levels are...
10.
Lavall D, Schuster P, Jacobs N, Kazakov A, Bohm M, Laufs U
J Biol Chem
. 2017 Mar;
292(18):7542-7553.
PMID: 28320863
The aim of the study was to characterize the role of Rac1 GTPase for the mineralocorticoid receptor (MR)-mediated pro-fibrotic remodeling. Transgenic mice with cardiac overexpression of constitutively active Rac1 (RacET)...