Abstract
The hedgehog (Hh) pathway is a sophisticated conserved cell signaling pathway that plays an essential role in controlling cell specification and proliferation, survival factors, and tissue patterning formation during embryonic development. Hh signal activity does not entirely disappear after development and may be reactivated in adulthood within tissue-injury-associated diseases, including idiopathic pulmonary fibrosis (IPF). The dysregulation of Hh-associated activating transcription factors, genomic abnormalities, and microenvironments is a co-factor that induces the initiation and progression of IPF.
Highlights
Cell signaling is a multifactorial system that represents the knot-like schematics of the signaling cascades that are used to transfer messages from the first messenger to the receptor and decoded through the signaling intermediates of the second messengers [1,2].Signal transduction, as an aspect of cell signaling, describes how cells interpret and react to external events [3]
Misharin et al revealed that the monocyte-derived alveolar macrophages (Mo-AMs) that persevere in the lung after injury resolution express higher proinflammatory and profibrotic genes than tissue-resident alveolar macrophages (TRAMs) [141]
The aberrant activation of Hh signaling is one of the core pathways that is involved in the development of pulmonary fibrosis
Summary
Cell signaling is a multifactorial system that represents the knot-like schematics of the signaling cascades that are used to transfer messages from the first messenger to the receptor and decoded through the signaling intermediates of the second messengers [1,2]. Hh is one of the major signal transduction networks for intercellular communication during embryonic development and organogenesis [4] and it regulates mitogenic and morphogenic functions during organ development [5]. The dysregulation of the Hh signaling network in controlled cell growth and division induces autocrine and paracrine function distortions, leading to the development of tumorigenesis and cancer progression [6,7]. Myofibroblast-associated Hh signaling is involved in accelerated tumor growth in various cancers [8–10]. Hh signaling is responsible for the development of numerous lung diseases [11]. Recent gene expression studies and animal disease models have demonstrated that Hh signaling can induce the fibroblast to myofibroblast transition (myofibroblast differentiation) in IPF [12].
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