Results 201 to 210 of about 296,542 (336)
NADPH oxidases in traumatic brain injury – Promising therapeutic targets?
Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Despite intense investigation, no neuroprotective agents for TBI have yet translated to the clinic.
Merry W. Ma+4 more
doaj
MicroRNAs in the Regulation of NADPH Oxidases in Vascular Diabetic and Ischemic Pathologies: A Case for Alternate Inhibitory Strategies? [PDF]
Wallace SR, Pagano PJ, Kračun D.
europepmc +1 more source
The regulatory effects of low‐intensity pulsed ultrasound (LIPUS) stimulation in senescent cells are presented. LIPUS perturbs the membrane in senescent cells and induces intracellular reactive oxygen species via NOX4 expression. Consequently, secretion of senescence‐associated secretory phenotype, followed by migration of monocytes/macrophages and ...
HyeRan Gwak+7 more
wiley +1 more source
The role of the host—Neutrophil biology
Abstract Neutrophilic polymorphonuclear leukocytes (neutrophils) are myeloid cells packed with lysosomal granules (hence also called granulocytes) that contain a formidable antimicrobial arsenal. They are terminally differentiated cells that play a critical role in acute and chronic inflammation, as well as in the resolution of inflammation and wound ...
Iain L. C. Chapple+4 more
wiley +1 more source
NADPH Oxidases in Diastolic Dysfunction and Heart Failure with Preserved Ejection Fraction. [PDF]
Teuber JP+4 more
europepmc +1 more source
NADPH oxidases and ROS signaling in the gastrointestinal tract
G. Aviello, U. Knaus
semanticscholar +1 more source
Model of LIF‐to‐aMYF reversible switch during fibrosis formation and resolution in old mice. The main contributors during fibrosis formation to Cthrc1+ aMYF are Acta2+ LIFhigh alveolar fibroblasts. During fibrosis resolution, Cthrc1+ aMYF differentiate back to the LIFhigh (please write "high" in superscript) alveolar fibroblasts cluster.
Arun Lingampally+18 more
wiley +1 more source
Adequate NADK/NADK2 level is essential to the proper functioning of redox and folate cycles and the purine biosynthesis pathway, and as well as maintenance of GSIS response. During aging, diminished NADK/NADK2 expression alters the metabolic status quo, increasing AICAR production. The latter activates AMPK and suppresses GSIS.
Guan‐Jie Li+6 more
wiley +1 more source
Enzymology of Ca2+-Mobilizing Second Messengers Derived from NAD: From NAD Glycohydrolases to (Dual) NADPH Oxidases. [PDF]
Guse AH.
europepmc +1 more source
Role of Src homology 3 domains in assembly and activation of the phagocyte NADPH oxidase.
Hidetoshi Sumimoto+8 more
openalex +1 more source