Year: 2020
Type: review
Abstract: Ion channels/pumps are essential regulators of innate immune cell function. Macrophages have been increasingly recognized to have phenotypic plasticity and location-specific functions in the lung. Transient receptor potential vanilloid 4 (TRPV4) function in lung injury has been shown to be stimulus- and cell-type specific. In the current review, we discuss the importance of TRPV4 in macrophages and its role in phagocytosis and cytokine secretion in acute lung injury/acute respiratory distress syndrome (ARDS). Furthermore, TRPV4 controls a MAPK molecular switch from predominately c-Jun N-terminal kinase, JNK activation, to that of p38 activation, that mediates phagocytosis and cytokine secretion in a matrix stiffness-dependent manner. Expanding knowledge regarding the downstream mechanisms by which TRPV4 acts to tailor macrophage function in pulmonary inflammatory diseases will allow for formulation of novel therapeutics.
Source: Frontiers in Immunology
Institutions: Cleveland Clinic, Cleveland Clinic Research
Language: English
Topic: Ion Channels and Receptors
Subfield: Sensory Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,950
Awards: Matrix-Myosin II Interactions Drive Fibrosis in Idiopathic Pulmonary Fibrosis., Transient Receptor Potential Vanilloid 4 (TRPV4) mediates the host defense and lung injury response to bacterial pneumonia, Myofibroblast differentiation and fibrosis are mediated by TRPV4 mechanosensing, TRPV4-PI3K Axis Mediates Pulmonary and Cardiac Fibrosis
OpenAlex ID: W3037600314