October 12, 2001Circulation Research
ERK and p38 MAPK, but not NF-κB, Are Critically Involved in Reactive Oxygen Species–Mediated Induction of IL-6 by Angiotensin II in Cardiac Fibroblasts
Key result
Angiotensin II stimulates reactive oxygen species production, activating MAPKs to induce IL-6 gene expression through a CRE-dependent, but not NF-kappaB-dependent, pathway in cardiac fibroblasts.
Population
Cardiac fibroblasts
Comparison
Angiotensin II vs Untreated control cells
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
Provides mechanistic detail on Ang II–IL-6 signaling in fibroblasts; extends prior observations but leaves open clinical translation.
Structured PICO
P
Population
Cardiac fibroblasts
I
Intervention
Angiotensin II (with or without inhibitors candesartan, diphenyleneiodonium [DPI], N-acetylcysteine, Tiron, PD98059, SB203580)
C
Comparator
Untreated control cells
O
Outcome
IL-6 gene expression and intracellular reactive oxygen species (ROS) levelssurrogate
Angiotensin II induces IL-6 expression in cardiac fibroblasts via ROS-mediated activation of ERK and p38 MAPK pathways, independent of NF-κB, providing mechanistic insights into Ang II-induced cardiac hypertrophy.
Cite This Study
Sano et al. (2001) studied Angiotensin II-induced cardiac hypertrophy. Angiotensin II and signaling inhibitors was evaluated on IL-6 gene expression and signaling pathway activation. Angiotensin II stimulates reactive oxygen species production, activating MAPKs to induce IL-6 gene expression through a CRE-dependent, but not NF-kappaB-dependent, pathway in cardiac fibroblasts.