Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

摘要: The transient activation of inflammatory networks is required for adipose tissue remodeling including the “browning” white fat in response to stimuli such as β3-adrenergic receptor activation. In this process, acquires thermogenic characteristics through recruitment so-called beige adipocytes. We investigated downstream signaling pathways impinging on adipocyte progenitors that promote de novo formation showed Jak family kinases controlled TGFβ microenvironment Stat3 and thereby adipogenic commitment, a function was differentiation murine human progenitors. Jak/Stat3 inhibited transcription factors Srf Smad3 by repressing local Tgfb3 Tgfb1 expression before core transcriptional cascade activated. This pathway cross-talk triggered stromal cells ATGL-dependent lipolysis wave IL-6 cytokines at onset induced stimulation. Our results provide insight into are relevant therapeutic targeting pathways.