ArticleAmerican journal of physiology. Heart and circulatory physiology2009
sGC(alpha)1(beta)1 attenuates cardiac dysfunction and mortality in murine inflammatory shock models.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Acute myocardial infarction and cardiogenic shock: prognostic impact of cytokines: INF-γ, TNF-α, MIP-1β, G-CSF, and MCP-1β.Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2012Trial
- Proteomic surveys of the mouse heart unveil cardiovascular responses to nitric oxide/cGMP signaling deficiencies.Communications biology · 2025Article
- Arterial Hypertension: Novel Pharmacological Targets and Future Perspectives.Journal of clinical medicine · 2024Review
- DNA-PKcs Phosphorylates Cofilin2 to Induce Endothelial Dysfunction and Microcirculatory Disorder in Endotoxemic Cardiomyopathy.Research (Washington, D.C.) · 2024Article
- Distinct Myocardial Mechanisms Underlie Cardiac Dysfunction in Endotoxemic Male and Female Mice.Shock (Augusta, Ga.) · 2016Article
- Androgen-sensitive hypertension associated with soluble guanylate cyclase-α1 deficiency is mediated by 20-HETE.American journal of physiology. Heart and circulatory physiology · 2016Article
- Cardiovascular and pharmacological implications of haem-deficient NO-unresponsive soluble guanylate cyclase knock-in mice.Nature communications · 2015Article
- Bone morphogenetic protein receptor type II deficiency and increased inflammatory cytokine production. A gateway to pulmonary arterial hypertension.American journal of respiratory and critical care medicine · 2015Article
- Nitrate/Nitrite as Critical Mediators to Limit Oxidative Injury and Inflammation.Antioxidants & redox signaling · 2015Review
- Extending the translational potential of targeting NO/cGMP-regulated pathways in the CVS.British journal of pharmacology · 2015Review
- Shedding of the tumor necrosis factor (TNF) receptor from the surface of hepatocytes during sepsis limits inflammation through cGMP signaling.Science signaling · 2015Article
- New insights into the role of soluble guanylate cyclase in blood pressure regulation.Current opinion in nephrology and hypertension · 2014Review
- Deletion of the murine cytochrome P450 Cyp2j locus by fused BAC-mediated recombination identifies a role for Cyp2j in the pulmonary vascular response to hypoxia.PLoS genetics · 2013Article
- Genetic modification of hypertension by sGCα1.Trends in cardiovascular medicine · 2013Review
- SERCA Cys674 sulphonylation and inhibition of L-type Ca2+ influx contribute to cardiac dysfunction in endotoxemic mice, independent of cGMP synthesis.American journal of physiology. Heart and circulatory physiology · 2013Article
- Soluble guanylate cyclase modulates alveolarization in the newborn lung.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Cellular basis of burn-induced cardiac dysfunction and prevention by mesenteric lymph duct ligation.The Journal of surgical research · 2013Article
- Analyzing left ventricular function in mice with Doppler echocardiography.Heart failure reviews · 2013Review
- Assessing murine resistance artery function using pressure myography.Journal of visualized experiments : JoVE · 2013Article
- Reduction of cardiomyocyte S-nitrosylation by S-nitrosoglutathione reductase protects against sepsis-induced myocardial depression.American journal of physiology. Heart and circulatory physiology · 2013Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Altered cGMP signaling has been implicated in myocardial depression, morbidity, and mortality associated with sepsis. Previous studies, using inhibitors of soluble guanylate cyclase (sGC), suggested that cGMP generated by sGC contributed to the cardiac dysfunction and mortality associated with sepsis. We used sGC(alpha)(1)-deficient (sGC(alpha)(1)(-/-)) mice to unequivocally determine the role of sGC(alpha)(1)beta(1) in the development of cardiac dysfunction and death associated with two models of inflammatory shock: endotoxin- and TNF-induced shock. At baseline, echocardiographic assessment and invasive hemodynamic measurements of left ventricular (LV) dimensions and function did not differ between wild-type (WT) mice and sGC(alpha)(1)(-/-) mice on the C57BL/6 background (sGC(alpha)(1)(-/-B6) mice). At 14 h after endotoxin challenge, cardiac dysfunction was more pronounced in sGC(alpha)(1)(-/-B6) than WT mice, as assessed using echocardiographic and hemodynamic indexes of LV function. Similarly, Ca(2+) handling and cell shortening were impaired to a greater extent in cardiomyocytes isolated from sGC(alpha)(1)(-/-B6) than WT mice after endotoxin challenge. Importantly, morbidity and mortality associated with inflammatory shock induced by endotoxin or TNF were increased in sGC(alpha)(1)(-/-B6) compared with WT mice. Together, these findings suggest that cGMP generated by sGC(alpha)(1)beta(1) protects against cardiac dysfunction and mortality in murine inflammatory shock models.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.