The study identifies a forward-feed loop involving macrophage-T cell interactions, IFN-γ, and MCP-1 that drives Ang II-induced cardiac inflammation and fibrosis.
Identifies macrophage-T cell feedback in Ang II fibrosis; leaves open translation to human hypertensive heart disease.
Reciprocal interaction between macrophages and T cells in heart stimulates IFN-γ expression, leading to increased MCP-1 expression in macrophages, which results a forward-feed recruitment of macrophages, thus contributing to Ang II-induced cardiac inflammation and fibrosis.
No takes yet. Share an insight, caveat, or question.
Han et al. (2012) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: