To examine the molecular mechanisms of occludin (OCLN) in cardiovascular and cerebrovascular diseases and explore specific therapeutic strategies targeting OCLN, such as enhancing its expression or function.
Key Findings:
OCLN is crucial for maintaining vascular endothelial barrier integrity.
Dysfunction of OCLN is linked to increased vascular permeability and exacerbation of diseases like ischemic stroke and atherosclerosis.
OCLN regulates signaling pathways such as NF-κB and MAPK, influencing inflammation and oxidative stress.
Recent studies suggest OCLN has roles in endothelial autophagy and metabolic reprogramming.
Interpretation:
OCLN's dysfunction significantly contributes to the pathophysiology of cardiovascular and cerebrovascular diseases, indicating its potential as a therapeutic target for intervention.
Limitations:
Controversies remain regarding the upstream and downstream regulatory networks of OCLN, such as the role of epigenetic modifications.
Tissue-specific expression differences and the feasibility of targeting OCLN therapeutically require further investigation, particularly in different vascular contexts.
Conclusion:
Targeting OCLN may offer new therapeutic strategies for repairing vascular barriers and modulating related signaling pathways in cardiovascular and cerebrovascular diseases, highlighting its importance in future research.
