scholarly journals Proteomic study of acute respiratory distress syndrome: current knowledge and implications for drug development

2016 ◽  
Vol 13 (5) ◽  
pp. 457-469 ◽  
Author(s):  
Joseph E. Levitt ◽  
Angela J. Rogers
2020 ◽  
Vol 10 (4) ◽  
pp. 204589402096535
Author(s):  
Pratap Karki ◽  
Konstantin G. Birukov ◽  
Anna A. Birukova

Extracellular histones released from injured or dying cells following trauma and other severe insults can act as potent damage-associated molecular patterns. In fact, elevated levels of histones are present in human circulation in hyperinflammatory states such as acute respiratory distress syndrome and sepsis. The molecular mechanisms owing to histone-induced pathologies are at the very beginning of elucidating. However, neutralization of histones with antibodies, histone-binding or histone-degrading proteins, and heparan sulfates have shown promising therapeutic effects in pre-clinical acute respiratory distress syndrome and sepsis models. Various cell types undergoing necrosis and apoptosis or activated neutrophils forming neutrophil extracellular traps have been implicated in excessive release of histones which further augments tissue injury and may culminate in multiple organ failure. At the molecular level, an uncontrolled inflammatory cascade has been considered as the major event; however, histone-activated coagulation and thrombosis represent additional pathologic events reflecting coagulopathy. Furthermore, epigenetic regulation and chemical modifications of circulating histones appear to be critically important in their biological functions as evidenced by increased cytotoxicity associated with citrullinated histone. Herein, we will briefly review the current knowledge on the role of histones in acute respiratory distress syndrome and sepsis, and discuss the future potential of anti-histone therapy for treatment of these life-threatening disorders.


2018 ◽  
Vol 104 (3) ◽  
pp. 484-494 ◽  
Author(s):  
Musaddique Hussain ◽  
Chengyun Xu ◽  
Mashaal Ahmad ◽  
Abdul Majeed ◽  
Meiping Lu ◽  
...  

Author(s):  
Inna Krynytska ◽  
Mariya Marushchak ◽  
Inna Birchenko ◽  
Alina Dovgalyuk ◽  
Oleksandr Tokarskyy

Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus, Severe Acute Respiratory Syndrome-Coronavi- rus-2 (SARS-CoV-2), led to the ongoing global public health crisis. Existing clinical data suggest that COVID-19 patients with acute respiratory distress syndrome (ARDS) have worse outcomes and increased risk of intensive care unit (ICU) admission. The rapid increase in the numbers of patients requiring ICU care may imply a sudden and major challenge for affected health care systems. In this narrative review, we aim to summarize current knowledge of pathophysiology, clinical and morphological characteristics of COVID-19-associated ARDS and ARDS caused by other factors (classical ARDS) as defined by Berlin criteria, and therefore to elucidate the differences, which can affect clinical management of COVID-19-as- sociated ARDS. Fully understanding the characteristics of COVID-19-associated ARDS will help identify its early progres- sion and tailor the treatment, leading to improved prognosis in severe cases and reduced mortality. The notable mechanisms of COVID-19-associated ARDS include severe pulmonary infiltration/edema and inflammation, leading to impaired alveolar homeostasis, alteration of pulmonary physiology resulting in pulmonary fibrosis, endothelial inflammation and vascular thrombosis. Despite some distinct differences between COVID-19-associated ARDS and classical ARDS as defined by Ber- lin criteria, general treatment principles, such as lung-protective ventilation and rehabilitation concepts should be applied whenever possible. At the same time, ventilatory settings for COVID-19-associated ARDS require to be adapted in individ- ual cases, depending on respiratory mechanics, recruitability and presentation timing.  


Biomedicines ◽  
2020 ◽  
Vol 8 (7) ◽  
pp. 230 ◽  
Author(s):  
Chuan-Mu Chen ◽  
Hsiao-Ching Lu ◽  
Yu-Tang Tung ◽  
Wei Chen

Acute respiratory distress syndrome (ARDS) is a common and devastating syndrome that contributes to serious morbidities and mortality in critically ill patients. No known pharmacologic therapy is beneficial in the treatment of ARDS, and the only effective management is through a protective lung strategy. Platelets play a crucial role in the pathogenesis of ARDS, and antiplatelet therapy may be a potential medication for ARDS. In this review, we introduce the overall pathogenesis of ARDS, and then focus on platelet-related mechanisms underlying the development of ARDS, including platelet adhesion to the injured vessel wall, platelet-leukocyte-endothelium interactions, platelet-related lipid mediators, and neutrophil extracellular traps. We further summarize antiplatelet therapy, including aspirin, glycoprotein IIb/IIIa receptor antagonists, and P2Y12 inhibitors for ARDS in experimental and clinical studies and a meta-analysis. Novel aspirin-derived agents, aspirin-triggered lipoxin, and aspirin-triggered resolvin D1 are also described here. In this narrative review, we summarize the current knowledge of the role of platelets in the pathogenesis of ARDS, and the potential benefits of antiplatelet therapy for the prevention and treatment of ARDS.


2021 ◽  
Vol 8 (4) ◽  
pp. 773
Author(s):  
Jade Irene Linardi

Coronavirus disease 2019 (COVID-19) as a global pandemic has become a major burden especially in the health care system and economy. COVID-19 has clinical presentations ranging from remain asymptomatic to severe acute respiratory distress syndrome (ARDS) and death. All age groups are susceptible to this virus, but it seems that children with COVID-19 have milder symptoms than adults. Neonates, however, have been reported to have more severe cases compared to older children. There is also a possibility of vertical transmission from mothers to their neonates which could not be ignored. This review provides current knowledge of COVID-19 in neonates.   


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