Results 41 to 50 of about 542,420 (309)

Oxidative stress-induced FABP5 S-glutathionylation protects against acute lung injury by suppressing inflammation in macrophages

open access: yesNature Communications, 2021
Oxidative stress contributes to the pathogenesis of acute lung injury. Protein S-glutathionylation plays an important role in cellular antioxidant defense. Here we report that the expression of deglutathionylation enzyme Grx1 is decreased in the lungs of
Yuxian Guo   +9 more
semanticscholar   +1 more source

The role of ubiquitination and deubiquitination in the regulation of cell junctions

open access: yesProtein & Cell, 2017
Maintenance of cell junctions plays a crucial role in the regulation of cellular functions including cell proliferation, permeability, and cell death.
Junting Cai   +3 more
doaj   +1 more source

Viral pathogens and acute lung injury: investigations inspired by the SARS epidemic and the 2009 H1N1 influenza pandemic. [PDF]

open access: yes, 2013
Acute viral pneumonia is an important cause of acute lung injury (ALI), although not enough is known about the exact incidence of viral infection in ALI.
Hendrickson, Carolyn M   +1 more
core   +2 more sources

Animal models of acute lung injury

open access: yesAmerican Journal of Physiology - Lung cellular and Molecular Physiology, 2008
Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi.
G. Matute-Bello, C. Frevert, T. Martin
semanticscholar   +1 more source

Novel anti-tumour necrosis factor receptor-1 (TNFR1) domain antibody prevents pulmonary inflammation in experimental acute lung injury. [PDF]

open access: yes, 2018
BACKGROUND: Tumour necrosis factor alpha (TNF-α) is a pleiotropic cytokine with both injurious and protective functions, which are thought to diverge at the level of its two cell surface receptors, TNFR1 and TNFR2.

core   +2 more sources

Gut-Lung Crosstalk in Sepsis-Induced Acute Lung Injury

open access: yesFrontiers in Microbiology, 2021
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common acute and severe cases of the respiratory system with complicated pathogenesis and high mortality.
Xin Zhou, Youxia Liao
semanticscholar   +1 more source

Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1

open access: yesAging, 2020
Acute lung injury (ALI) is a syndrome associated with a high mortality rate. Nrf2 is a key regulator of intracellular oxidation homeostasis that plays a pivotal role in controlling lipid peroxidation, which is closely related to the process of ...
H. Dong   +6 more
semanticscholar   +1 more source

Inflammatory Caspases Drive Pyroptosis in Acute Lung Injury

open access: yesFrontiers in Pharmacology, 2021
Acute lung injury (ALI), a critical respiratory disorder that causes diffuse alveolar injury leads to high mortality rates with no effective treatment. ALI is characterized by varying degrees of ventilation/perfusion mismatch, severe hypoxemia, and poor ...
Bohao Liu   +6 more
semanticscholar   +1 more source

Obesity-induced adipokine imbalance impairs mouse pulmonary vascular endothelial function and primes the lung for injury. [PDF]

open access: yes, 2015
Obesity is a risk factor for the development of acute respiratory distress syndrome (ARDS) but mechanisms mediating this association are unknown. While obesity is known to impair systemic blood vessel function, and predisposes to systemic vascular ...
Duong, Michelle   +10 more
core   +2 more sources

The SARS-CoV-2 spike protein subunit S1 induces COVID-19-like acute lung injury in Κ18-hACE2 transgenic mice and barrier dysfunction in human endothelial cells

open access: yesAmerican Journal of Physiology - Lung cellular and Molecular Physiology, 2021
Acute lung injury (ALI) leading to acute respiratory distress syndrome is the major cause of COVID-19 lethality. Cell entry of SARS-CoV-2 occurs via the interaction between its surface spike protein (SP) and angiotensin-converting enzyme-2 (ACE2).
R. C. Colunga Biancatelli   +5 more
semanticscholar   +1 more source

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