Key result
In human aortic dissection tissue, STAT3 activation positively correlated with adventitial neutrophil infiltration (p=0.0002), suggesting involvement in tissue-destructive inflammation.
Why the study?
Activation status of inflammatory signaling and its relation to inflammatory cell infiltration are poorly characterized in human aortic dissection.
Observational (n=7)
No
p-value: p=0.0002
STAT3 activation correlates with adventitial neutrophil infiltration in human acute aortic dissection, suggesting a role for the STAT3 inflammatory pathway in AD pathogenesis.
STAT3-neutrophil correlation in dissection tissue is hypothesis-generating; leaves open targeted inhibition pending mechanistic validation.
Objective: Aortic dissection (AD) is a fatal disease that is caused by the rapid destruction of the aortic wall. Although recent studies in animal models indicate an important relationship between inflammation and tissue destruction, activation status of inflammatory signaling and its relation to the inflammatory cell infiltration are poorly characterized in human AD.
No takes yet. Share an insight, caveat, or question.
Yoshida et al. (2019) conducted an observational in Aortic Dissection (n=7). Acute type A aortic dissection vs. Aorta without dissection was evaluated on Correlation between STAT3 activation and neutrophil infiltration in the adventitial layer (p=0.0002). In human aortic dissection tissue, STAT3 activation positively correlated with adventitial neutrophil infiltration (p=0.0002), suggesting involvement in tissue-destructive inflammation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: