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- W4317504549 endingPage "153" @default.
- W4317504549 startingPage "153" @default.
- W4317504549 abstract "Inflammation is a hallmark of the physiological response to aggressions. It is orchestrated by a plethora of molecules that detect the danger, signal intracellularly, and activate immune mechanisms to fight the threat. Understanding these processes at a level that allows to modulate their fate in a pathological context strongly relies on in vivo studies, as these can capture the complexity of the whole process and integrate the intricate interplay between the cellular and molecular actors of inflammation. Over the years, zebrafish has proven to be a well-recognized model to study immune responses linked to human physiopathology. We here provide a systematic review of the molecular effectors of inflammation known in this vertebrate and recapitulate their modes of action, as inferred from sterile or infection-based inflammatory models. We present a comprehensive analysis of their sequence, expression, and tissue distribution and summarize the tools that have been developed to study their function. We further highlight how these tools helped gain insights into the mechanisms of immune cell activation, induction, or resolution of inflammation, by uncovering downstream receptors and signaling pathways. These progresses pave the way for more refined models of inflammation, mimicking human diseases and enabling drug development using zebrafish models." @default.
- W4317504549 created "2023-01-20" @default.
- W4317504549 creator A5008593596 @default.
- W4317504549 creator A5022255682 @default.
- W4317504549 creator A5038856853 @default.
- W4317504549 creator A5044306189 @default.
- W4317504549 creator A5084525465 @default.
- W4317504549 creator A5085630623 @default.
- W4317504549 creator A5086359802 @default.
- W4317504549 date "2023-01-19" @default.
- W4317504549 modified "2023-10-01" @default.
- W4317504549 title "Molecular Actors of Inflammation and Their Signaling Pathways: Mechanistic Insights from Zebrafish" @default.
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