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20180041@wnmc.edu.cnMitochondrial autophagy is essential for maintaining mitochondrial health by selectively degrading damaged mitochondria. This process involves two main pathways: ubiquitin-dependent and ubiquitin-independent autophagy.
Sepsis causes organ dysfunction due to infection, with acute lung injury (ALI) being a common secondary condition. ALI is characterized by excessive inflammation in the lungs, leading to mitochondrial dysfunction.
Understanding the mechanisms of mitochondrial autophagy can provide new insights for treating sepsis-associated ALI. Continued research could identify novel therapeutic targets to improve outcomes for patients with ALI and sepsis.
In the early stages of sepsis-related ALI, mitochondrial autophagy is enhanced. In severe or prolonged cases, excessive mitochondrial autophagy may occur. In the later stages, particularly in severe or chronic cases, mitochondrial autophagy may be impaired or completely lost.
Mitochondrial autophagy holds therapeutic potential for the perioperative assessment and management of sepsis-related ALI. Further investigation into this potential is warranted.
Open Access20180041@wnmc.edu.cnMitochondrial autophagy is essential for maintaining mitochondrial health by selectively degrading damaged mitochondria. This process involves two main pathways: ubiquitin-dependent and ubiquitin-independent autophagy.
Sepsis causes organ dysfunction due to infection, with acute lung injury (ALI) being a common secondary condition. ALI is characterized by excessive inflammation in the lungs, leading to mitochondrial dysfunction.
Understanding the mechanisms of mitochondrial autophagy can provide new insights for treating sepsis-associated ALI. Continued research could identify novel therapeutic targets to improve outcomes for patients with ALI and sepsis.
In the early stages of sepsis-related ALI, mitochondrial autophagy is enhanced. In severe or prolonged cases, excessive mitochondrial autophagy may occur. In the later stages, particularly in severe or chronic cases, mitochondrial autophagy may be impaired or completely lost.
Mitochondrial autophagy holds therapeutic potential for the perioperative assessment and management of sepsis-related ALI. Further investigation into this potential is warranted.
Sepsis is a systemic inflammatory response syndrome caused by infection, leading to acute lung injury and acute respiratory distress syndrome, which are common life-threatening complications in intensive care units. Mitochondrial autophagy, a process that selectively removes damaged mitochondria, is essential for maintaining the stability of the intracellular environment and cellular function. In recent years, the role of mitochondrial autophagy in sepsis-associated acute lung injury and acute respiratory distress syndrome has garnered significant attention. This review summarizes the research progress of mitochondrial autophagy in sepsis-associated acute lung injury and acute respiratory distress syndrome, focusing on its mechanism, influencing factors, and potential therapeutic agents.
ISSN: 2957-5443
Volume 3, Issue 1
March 2025
Pages: 1-38
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