Abstract
Bone morphogenetic proteins (BMPs) comprise a major subgroup of the transforming growth factor (TGF)-β superfamily. They play pivotal roles in embryonic development and tissue homeostasis in adults. Deregulation of BMP and TGF-β signaling contributes to developmental anomalies and multiple diseases. In this mini-review, we focus on BMP signaling in inflammatory disorders of the pancreas, acute and chronic pancreatitis, in contrast to TGF-β signaling. We then discuss molecular mechanisms that interact with and connect between the BMP and TGF-β signaling pathways. Lastly, we review potential implications of these molecular mechanisms for therapeutic development. In summary, BMP signaling pathway plays different roles during pancreatitis disease development, and the antagonism between BMP and TGF-β signaling can be manipulated for therapeutic development against pancreatitis.
Highlights
Bone morphogenetic proteins (BMPs) constitute a major subgroup of the transforming growth factor (TGF)-β superfamily, comprising 18 out of the total 33 members [1]
Knockout of BMPR2 in mice exacerbates chronic pancreatitis (CP), leading to enhanced inflammation and fibrosis, two hallmarks of CP [24]. These findings reveal a protective and anti-fibrogenic role of BMP signaling in CP, in contrast to the pro-fibrogenic Transforming Growth Factor-Beta (TGF-β) signaling [25,26]
To search for molecular links between BMP and TGF-β, we focus on Gremlin1 (Grem1), a BMP antagonist, which has reported pro-fibrogenic function in several organs [15,27,28]
Summary
Bone morphogenetic proteins (BMPs) constitute a major subgroup of the transforming growth factor (TGF)-β superfamily, comprising 18 (several named as growth differentiation factors) out of the total 33 members [1]. In the canonical signaling pathway, BMP ligand binds to BMP receptors type I (BMPR1) and type II (BMPR2) on the cell surface and subsequently activates intracellular mediators Smad1/5/8 via phosphorylation [3]. Activation of specific Smads may lead to distinct or opposing biological outcomes, most notably in disease states [3,6,7].
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