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Targeting Soluble Guanylyl Cyclase during Ischemia and Reperfusion [PDF]

open access: yesCells, 2023
Ischemia and reperfusion (IR) damage organs and contribute to many disease states. Few effective treatments exist that attenuate IR injury. The augmentation of nitric oxide (NO) signaling remains a promising therapeutic target for IR injury.
Eric H. Mace   +3 more
doaj   +4 more sources

Effects of soluble guanylyl cyclase stimulation on muscle oxygenation and exercise capacity in heart failure with mildly reduced ejection fraction [PDF]

open access: yesExperimental Physiology
Heart failure (HF) with a mildly reduced ejection fraction (HFmrEF; 40%–49%) is present in ≤25% of HF patients. Therapeutic treatment options for HFmrEF‐associated exercise intolerance are limited.
Ramona E. Weber   +10 more
doaj   +3 more sources

Soluble guanylyl cyclase mediates noncanonical nitric oxide signaling by nitrosothiol transfer under oxidative stress [PDF]

open access: goldRedox Biology, 2022
Soluble guanylyl cyclase (GC1) is an α/β heterodimer producing cGMP when stimulated by nitric oxide (NO). The NO-GC1-cGMP pathway is essential for cardiovascular homeostasis but is disrupted by oxidative stress, which causes GC1 desensitization to NO by ...
Chuanlong Cui   +5 more
doaj   +3 more sources

Soluble Guanylyl Cyclase Activators—Promising Therapeutic Option in the Pharmacotherapy of Heart Failure and Pulmonary Hypertension [PDF]

open access: yesMolecules, 2023
Endogenous nitric oxide (NO)-dependent vascular relaxation plays a leading role in the homeostasis of the cardiovascular, pulmonary, and vascular systems and organs, such as the kidneys, brain, and liver.
Grzegorz Grześk   +6 more
doaj   +2 more sources

Stimulation of Erythrocyte Soluble Guanylyl Cyclase Induces cGMP Export and Cardioprotection in Type 2 Diabetes [PDF]

open access: yesJACC: Basic to Translational Science, 2023
Summary: Reduced nitric oxide (NO) bioactivity in red blood cells (RBCs) is critical for augmented myocardial ischemia-reperfusion injury in type 2 diabetes.
Tong Jiao, MD, PhD   +10 more
doaj   +2 more sources

The soluble guanylyl cyclase activator bay 58-2667 selectively limits cardiomyocyte hypertrophy. [PDF]

open access: goldPLoS ONE, 2012
Although evidence now suggests cGMP is a negative regulator of cardiac hypertrophy, the direct consequences of the soluble guanylyl cyclase (sGC) activator BAY 58-2667 on cardiac remodeling, independent of changes in hemodynamic load, has not been ...
Jennifer C Irvine   +7 more
doaj   +3 more sources

Nitroxyl (HNO) stimulates soluble guanylyl cyclase to suppress cardiomyocyte hypertrophy and superoxide generation. [PDF]

open access: goldPLoS ONE, 2012
New therapeutic targets for cardiac hypertrophy, an independent risk factor for heart failure and death, are essential. HNO is a novel redox sibling of NO• attracting considerable attention for the treatment of cardiovascular disorders, eliciting cGMP ...
Eliane Q Lin   +9 more
doaj   +3 more sources

Soluble guanylyl cyclase: Molecular basis for ligand selectivity and action in vitro and in vivo [PDF]

open access: yesFrontiers in Molecular Biosciences, 2022
Nitric oxide (NO), carbon monoxide (CO), oxygen (O2), hydrogen sulfide (H2S) are gaseous molecules that play important roles in the physiology and pathophysiology of eukaryotes.
Gang Wu, Iraida Sharina, Emil Martin
doaj   +2 more sources

Cellular Factors That Shape the Activity or Function of Nitric Oxide-Stimulated Soluble Guanylyl Cyclase [PDF]

open access: yesCells, 2023
NO-stimulated guanylyl cyclase (SGC) is a hemoprotein that plays key roles in various physiological functions. SGC is a typical enzyme-linked receptor that combines the functions of a sensor for NO gas and cGMP generator.
Iraida Sharina, Emil Martin
doaj   +2 more sources

Inhibitory Peptide of Soluble Guanylyl Cyclase/Trx1 Interface Blunts the Dual Redox Signaling Functions of the Complex [PDF]

open access: yesAntioxidants, 2023
Soluble guanylyl cyclase (GC1) and oxido-reductase thioredoxin (Trx1) form a complex that mediates two NO signaling pathways as a function of the redox state of cells.
Chuanlong Cui   +5 more
doaj   +2 more sources

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