The Role of Histone Deacetylases in Acute Lung Injury-Friend or Foe.
Guoqing LuoBohao LiuTinglv FuYi LiuBoyang LiNing LiQing GengPublished in: International journal of molecular sciences (2023)
Acute lung injury (ALI), caused by intrapulmonary or extrapulmonary factors such as pneumonia, shock, and sepsis, eventually disrupts the alveolar-capillary barrier, resulting in diffuse pulmonary oedema and microatasis, manifested by refractory hypoxemia, and respiratory distress. Not only is ALI highly lethal, but even if a patient survives, there are also multiple sequelae. Currently, there is no better treatment than supportive care, and we urgently need to find new targets to improve ALI. Histone deacetylases (HDACs) are epigenetically important enzymes that, together with histone acetylases (HATs), regulate the acetylation levels of histones and non-histones. While HDAC inhibitors (HDACis) play a therapeutic role in cancer, inflammatory, and neurodegenerative diseases, there is also a large body of evidence suggesting the potential of HDACs as therapeutic targets in ALI. This review explores the unique mechanisms of HDACs in different cell types of ALI, including macrophages, pulmonary vascular endothelial cells (VECs), alveolar epithelial cells (AECs), and neutrophils.
Keyphrases
- dna methylation
- endothelial cells
- lipopolysaccharide induced
- pulmonary hypertension
- lps induced
- healthcare
- intensive care unit
- oxidative stress
- histone deacetylase
- papillary thyroid
- palliative care
- case report
- acute kidney injury
- stem cells
- quality improvement
- gene expression
- human health
- pain management
- chronic pain
- septic shock
- mesenchymal stem cells
- lymph node metastasis
- climate change
- high glucose
- childhood cancer
- affordable care act
- acute respiratory distress syndrome