Abstract

BACKGROUND: Acute respiratory distress syndrome (ARDS), which is characterized by severe hypoxemia (PaO2/FIO2 ≤300 mmHg), is usually companied by uncontrolled inflammation, oxidative injury, and the damage to the alveolar-capillary barrier. Severe ARDS is usually companied with acute lung injury that worsen the patients’ condition. HIPK1 is a modulator of homeodomain-containing transcription factors and regulates multiple cellular biological process associated with inflammation and anti-stress responses.

MATERIAL AND METHODS: We used an LPS-induced mouse acute lung injury (ALI) model to investigate the possible role of HIPK1 in ALI pathophysiology.

RESULTS: We found the HIPK1 was elevated in ALI model mice while interference of HIPK1 by siRNA attenuated the inflammation and oxidative stress indicators (H2O2, O–2, and NO). Further research found HIPK1 interference enhanced the autophagy.

CONCLUSIONS: Decreased HIPK1 in ALI showed protective effects in attenuating inflammation and oxidative stress and enhancing autophagy, indicating HIPK1 as a possible target in ALI management.

Keywords: acute lung injury, Carrier Proteins, Interleukin-6, Lipopolysaccharides, Lung, Mice, Inbred C57BL, Protein Kinases, Protein Serine-Threonine Kinases, respiratory distress syndrome