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Autophagy in Acute Lung Injury

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Date 2024 Nov 11
PMID 39527232
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Abstract

Acute lung injury (ALI) is a critical condition marked by rapid-onset respiratory failure due to extensive inflammation and increased pulmonary vascular permeability, often progressing to acute respiratory distress syndrome (ARDS) with high mortality. Autophagy, a cellular degradation process essential for removing damaged organelles and proteins, plays a crucial role in regulating lung injury and repair. This review examines the protective role of autophagy in maintaining cellular function and reducing inflammation and oxidative stress in ALI. It underscores the necessity of precise regulation to fully harness the therapeutic potential of autophagy in this context. We summarize the mechanisms by which autophagy influences lung injury and repair, discuss the interplay between autophagy and apoptosis, and examine potential therapeutic strategies, including autophagy inducers, targeted autophagy signaling pathways, antioxidants, anti-inflammatory drugs, gene editing, and stem cell therapy. Understanding the role of autophagy in ALI could lead to novel interventions for improving patient outcomes and reducing mortality rates associated with this severe condition.

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