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10.3389/fphys.2022.828093

http://scihub22266oqcxt.onion/10.3389/fphys.2022.828093
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35431977!9008570!35431977
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suck abstract from ncbi


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pmid35431977      Front+Physiol 2022 ; 13 (ä): 828093
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  • Endothelial Transcytosis in Acute Lung Injury: Emerging Mechanisms and Therapeutic Approaches #MMPMID35431977
  • Jones JH; Minshall RD
  • Front Physiol 2022[]; 13 (ä): 828093 PMID35431977show ga
  • Acute Lung Injury (ALI) is characterized by widespread inflammation which in its severe form, Acute Respiratory Distress Syndrome (ARDS), leads to compromise in respiration causing hypoxemia and death in a substantial number of affected individuals. Loss of endothelial barrier integrity, pneumocyte necrosis, and circulating leukocyte recruitment into the injured lung are recognized mechanisms that contribute to the progression of ALI/ARDS. Additionally, damage to the pulmonary microvasculature by Gram-negative and positive bacteria or viruses (e.g., Escherichia coli, SARS-Cov-2) leads to increased protein and fluid permeability and interstitial edema, further impairing lung function. While most of the vascular leakage is attributed to loss of inter-endothelial junctional integrity, studies in animal models suggest that transendothelial transport of protein through caveolar vesicles, known as transcytosis, occurs in the early phase of ALI/ARDS. Here, we discuss the role of transcytosis in healthy and injured endothelium and highlight recent studies that have contributed to our understanding of the process during ALI/ARDS. We also cover potential approaches that utilize caveolar transport to deliver therapeutics to the lungs which may prevent further injury or improve recovery.
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