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Karl Swärd

Researcher at Lund University

Publications -  116
Citations -  9100

Karl Swärd is an academic researcher from Lund University. The author has contributed to research in topics: Vascular smooth muscle & Caveolae. The author has an hindex of 33, co-authored 110 publications receiving 8195 citations. Previous affiliations of Karl Swärd include University of Copenhagen & Canadian Institutes of Health Research.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Deletion of the G Protein-Coupled Receptor 30 Impairs Glucose Tolerance, Reduces Bone Growth, Increases Blood Pressure, and Eliminates Estradiol-Stimulated Insulin Release in Female Mice

Ulrika E.A. Mårtensson, +18 more
- 01 Feb 2009 - 
TL;DR: The findings show that GPR30 is important for several metabolic functions in female mice, including estradiol-stimulated insulin release, which is associated with decreased insulin expression and release in vivo and in vitro in isolated pancreatic islets.
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Cholesterol Depletion Impairs Vascular Reactivity to Endothelin-1 by Reducing Store-Operated Ca2+ Entry Dependent on TRPC1

Andreas Bergdahl, +8 more
- 31 Oct 2003 - 
TL;DR: It is suggested that cholesterol influences vascular reactivity to ET-1 by affecting the caveolar localization of TRPC1 through manipulating membrane cholesterol and disrupting caveolae in intact rat arteries.
Journal ArticleDOI

Inhibition of Rho-associated kinase blocks agonist-induced Ca2+ sensitization of myosin phosphorylation and force in guinea-pig ileum

Karl Swärd, +5 more
- 01 Jan 2000 - 
TL;DR: Results indicate that ROK mediates agonist‐induced increases in myosin phosphorylation and force by inhibiting MLCP activity throughosphorylation of MYPT.
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Cholesterol Depletion Disrupts Caveolae and Differentially Impairs Agonist-Induced Arterial Contraction

Karl Dreja, +5 more
- 01 Aug 2002 - 
TL;DR: Results show that a subset of signaling pathways that regulate smooth muscle contraction depends specifically on cholesterol, and the cholesterol-dependent step in serotonergic signaling occurs early in the pathway and depends on the integrity of caveolae.