Results 151 to 160 of about 95,947 (261)

IL‐33 Drives Inflammatory Changes and Extracellular Trap Formation in Eosinophils Involving Oxidised LDL and Complement Pathways

open access: yesAllergy, EarlyView.
IL‐33 induces inflammatory gene signatures in eosinophils, characterised by the upregulation of cell surface markers, inflammatory mediators and regulatory factors, all of which were also observed in nasal polyp‐derived eosinophils. Ox‐LDL and complement fragments (C3a and C5a) promote eosinophil adhesion and survival.
Emiko Matsuyama   +16 more
wiley   +1 more source

Umbilical Cord Blood–Derived Extracellular Vesicles Enhance Neurovascular Regeneration and Improve Erectile Function in a Mouse Model of Bilateral Cavernous Nerve Injury

open access: yesAndrology, EarlyView.
ABSTRACT Background Erectile dysfunction (ED) secondary to cavernous nerve injury (CNI), such as that occurring after radical prostatectomy, remains a significant clinical challenge, particularly among patients who do not respond to phosphodiesterase Type 5 inhibitors (PDE5i).
Minh Nhat Vo   +6 more
wiley   +1 more source

NADPH oxidase isoform NOX-2 deficiency affects mitochondrial oxygen consumption and metabolic flexibility. [PDF]

open access: yesRedox Biol
Thetchinamoorthy K   +6 more
europepmc   +1 more source

Non‐canonical PKG1 regulation in cardiovascular health and disease

open access: yesBritish Journal of Pharmacology, EarlyView.
It is well established that the cyclic GMP‐dependent protein kinase I (PKG1) is canonically activated by cyclic guanosine monophosphate (cGMP), enabling its regulation of vascular tone, cardiac function and smooth muscle homeostasis. However, diverse non‐canonical stimuli of PKG1 have also been identified.
Jie Su, Joseph Robert Burgoyne
wiley   +1 more source

Renal‐vascular axis: unmasking its role in vascular endothelial growth factor‐inhibitor vascular toxicity in cancer patients

open access: yesBritish Journal of Pharmacology, EarlyView.
Abstract Vascular toxicity is a growing concern in cancer patients receiving vascular endothelial growth factor inhibitor (VEGFi) therapy, posing a significant threat to patient prognosis. While the primary mechanism of VEGFi‐induced vascular toxicity is linked to redox‐sensitive reactions that disrupt vascular tone, leading to hypertension and ...
Grace Whelan, Karla B. Neves
wiley   +1 more source

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