Key result
Innate immune molecules in cardiac parenchymal cells influence homeostasis and cardiac remodelling through reprogrammed signalling pathways independent of conventional innate immune signalling.
Innate immune molecules in cardiac parenchymal cells influence cardiac homeostasis through reprogrammed signaling pathways, offering new insights into the pathogenesis of cardiac remodeling.
Canonical innate immune signalling involves complex cascades: multiple germline-encoded pattern recognition receptors rapidly recognize pathogen-associated or damage-associated molecular patterns to induce the production of cytokines, which bind to their corresponding receptors to orchestrate subsequent host defense phases. Inflammation is a healthy response to pathogenic signals, which are typically rapid and specific, and they terminate once the threat has passed. However, excessive activation or suppression of innate immune or inflammatory responses can lead to considerable human suffering, such as cardiac remodelling. Interestingly, recent studies have revealed that innate immune molecules in the parenchymal cells of the heart influence cardiac homeostasis not only by directly regulating innate immune responses but also through reprogrammed signalling pathways, which are independent of conventional innate immune signalling. Elucidating 'innate immune signalling reprogramming' events will help us better understand the functions of innate immune molecules and, moreover, the pathogenesis of cardiac diseases.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2017) conducted a review in Cardiac remodelling. Innate immune signalling was evaluated. Innate immune molecules in cardiac parenchymal cells influence homeostasis and cardiac remodelling through reprogrammed signalling pathways independent of conventional innate immune signalling.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: