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Carsten Lindschau

Researcher at Hannover Medical School

Publications -  80
Citations -  7210

Carsten Lindschau is an academic researcher from Hannover Medical School. The author has contributed to research in topics: Protein kinase C & Vascular smooth muscle. The author has an hindex of 44, co-authored 80 publications receiving 6921 citations. Previous affiliations of Carsten Lindschau include Charité & Free University of Berlin.

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Loss of Caveolae, Vascular Dysfunction, and Pulmonary Defects in Caveolin-1 Gene-Disrupted Mice

TL;DR: By targeted disruption of caveolin-1, the main protein component of caveolae, mice that lacked Caveolae were generated, causing aberrations in endothelium-dependent relaxation, contractility, and maintenance of myogenic tone and indicating a fundamental role in organizing multiple signaling pathways in the cell.
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Patients with preeclampsia develop agonistic autoantibodies against the angiotensin AT1 receptor.

TL;DR: It is suggested that preeclamptic patients develop stimulatory autoantibodies against the second extracellular AT1 receptor loop, which appears to be PKC-mediated and may participate in the angiotensin II-induced vascular lesions in these patients.
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From totipotent embryonic stem cells to spontaneously contracting smooth muscle cells: a retinoic acid and db-cAMP in vitro differentiation model.

TL;DR: A retinoic acid + db‐cAMP‐inducible embryonic stem cell model of in vitro vasculogenesis and ES cell‐derived cells expressing VSMC‐specific MHC and functional VSMC properties may be a suitable system to study mechanisms of VSMC differentiation.
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Aldosterone Potentiates Angiotensin II-Induced Signaling in Vascular Smooth Muscle Cells

TL;DR: Oxygen radicals, the MR, and the EGFR play a role in early signaling induced by Ang II and Ald in VSMCs and may help explain the effects of MR blockade on Ang II–induced end-organ damage in vivo.
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High Glucose Concentrations Increase Endothelial Cell Permeability via Activation of Protein Kinase Cα

TL;DR: It is concluded that an increase in extracellular glucose leads to a rapid dose-dependent increase in endothelial cell permeability via the activiation of PKC and that this effect is mediated by the PKC isoform alpha.