Application of FUNDC1 in treating acute respiratory distress syndrome and belongs to technical field of biology

A technology of FUNDC1, 1.FUNDC1, applied in the field of application in the treatment of acute respiratory distress syndrome, capable of solving damage, sepsis organs and other problems
CN111135289APending Publication Date: 2020-05-12PEKING UNION MEDICAL COLLEGE HOSPITAL CHINESE ACAD OF MEDICAL SCI
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Patent Information

Authority / Receiving Office
CN · China
Current Assignee / Owner
PEKING UNION MEDICAL COLLEGE HOSPITAL CHINESE ACAD OF MEDICAL SCI
Publication Date
2020-05-12

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Abstract

The invention discloses an application of FUNDC1 in treating acute respiratory distress syndrome and belongs to the technical field of biology. The present invention provides the application of the FUNDC1 in preparing products for preventing and / or treating inflammatory diseases. The mechanism of the FUNDC1 in preventing and / or treating inflammatory diseases is mainly to reduce lung injury by mediating mitochondrial autophagy to inhibit activation and expansion of inflammatory reactions induced by an ROS-NLRP3 signaling pathway. The invention provides the application of the FUNDC1 in preparingproduct for preventing and / or treating acute respiratory distress syndrome. The product provided by the invention can reduce lung injury by inhibiting inflammatory reactions by promoting autophagy during ARDS period. The FUNDC1 is expected to become a new target for ARDS treatment and has a wide application prospect.
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Description

technical field

[0001] The invention relates to the field of biotechnology, in particular to the application of FUNDC1 in the treatment of acute respiratory distress syndrome. Background technique

[0002] The etiology of acute respiratory distress syndrome (ARDS) is complex, and its pathogenesis has not been fully elucidated. Numerous studies have shown that the inflammatory response in the lung is the most important cause of ALI / ARDS. The activation of innate and adaptive immunity leads to a series of inflammatory responses, and the release of a large number of cytokines and inflammatory mediators leads to the aggravation of lung injury. The end result of this uncontrolled inflammatory response in the lung is damage to alveolar epithelial cells (AEC) and capillary endothelial cells, which in turn leads to alveolar hemorrhage, pulmonary edema formation, and hyaline membrane production.

[0003] Autophagy is a lysosome-dependent biological process for degrading intracellul...

Claims

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