Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The adverse cardiopulmonary phenotype of caveolin-1 deficient mice is mediated by a dysfunctional endothelium.

Journal of molecular and cellular cardiology - 1 May 2008

Wunderlich Carsten, Schober Kristin, Schmeisser Alexander, Heerwagen Christian, Tausche Anne-Kathrin, Steinbronn Nadine, Brandt Aljoscha, Kasper Michael, Schwencke Carsten, Braun-Dullaeus Ruediger C, Strasser Ruth H

Abstract excerpt

Recently generated caveolin-1 deficient mice (cav-1(-/-)) display several physiological alterations such as severe heart failure and lung fibrosis. The molecular mechanisms how the loss of caveolin-1 (cav-1) mediates these alterations are currently under debate. A plethora of studies support a role of cav-1 as a negative regulator of endothelial nitric oxide synthase (eNOS). Accordingly, constitutive eNOS...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Biopterins
Share to Caveolin 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dietary Supplements

Share to Heart Function Tests

Share to Hypertension, Pulmonary

Share to Lung Diseases

Share to Nitric Oxide

Share to Nitric Oxide Synthase Type III

Source

Identifiers

PMID: 18417152
DOI: 10.1016/j.yjmcc.2008.02.275

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The adverse cardiopulmonary phenotype of caveolin-1 deficient mice is mediated by a dysfunctional endothelium.PMID 18417152Read ↗

Chronic NOS inhibition prevents adverse lung remodeling and pulmonary arterial hypertension in caveolin-1 knockout mice.Semantic proximity Read ↗

Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities.Semantic proximity Read ↗

Reexpression of caveolin-1 in endothelium rescues the vascular, cardiac, and pulmonary defects in global caveolin-1 knockout mice.Semantic proximity Read ↗

Caveolae and caveolins in the cardiovascular system.Semantic proximity Read ↗

Regulation of NO Synthesis by Caveolin-1: A Review of Its Importance in Blood Vessels, Perivascular Adipose Tissue and in AtherosclerosisSemantic proximity Read ↗

Getting rid of caveolins: phenotypes of caveolin-deficient animals.Semantic proximity Read ↗

Disruption of Physiological Balance Between Nitric Oxide and Endothelium-Dependent Hyperpolarization Impairs Cardiovascular Homeostasis in Mice.Semantic proximity Read ↗

Genetic Ablation of Caveolin-1 Confers Protection Against AtherosclerosisSemantic proximity Read ↗

Do studies in caveolin-knockouts teach us about physiology and pharmacology or instead, the ways mice compensate for 'lost proteins'?Semantic proximity Read ↗

Caveolin-1/3 double-knockout mice are viable, but lack both muscle and non-muscle caveolae, and develop a severe cardiomyopathic phenotype.Semantic proximity Read ↗

Dexrazoxane prevents the development of the impaired cardiac phenotype in caveolin-1-disrupted mice.Semantic proximity Read ↗

Caveolin-deficient mice: insights into caveolar function human disease.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.