The Role of MAP Kinases in Trauma and Ischemia–Reperfusion
Edwin W. Lai, Luis H. Toledo‐Pereyra, Jon Walsh, Fernando López-Neblina, Roberto Anaya‐Prado
Abstract
Edwin W. Lai, Luis H. Toledo‐Pereyra, Jon Walsh, Fernando López-Neblina, Roberto Anaya‐Prado
Abstract
Mitogen-activated protein kinases (MAPKs) have been the focus of a number of studies, as these compounds are involved in a number of important inflammatory cell signaling mechanisms. Recent studies have further elucidated the role of MAPKs in the inflammatory response, as a result of trauma and/or ischemia–reperfusion (I/R) injury. There are three major classes of MAPKs that may be involved in the inflammatory response: extracellular signal-regulated kinases (ERKs), stress-activated protein kinases (SAPKs)/c-Jun NH2-terminal kinases (JNKs), and p38 MAPKs (p38). This is clinically relevant, because these pathways may be a possible target for anti-inflammatory drug intervention. This review studies the role of MAPKs in trauma and/or I/R.
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Mitogen-activated protein kinases (MAPKs) have been the focus of a number of studies, as these compounds are involved in a number of important inflammatory cell signaling mechanisms. Recent studies have further elucidated the role of MAPKs in the inflammatory response, as a result of trauma and/or ischemia–reperfusion (I/R) injury. There are three major classes of MAPKs that may be involved in the inflammatory response: extracellular signal-regulated kinases (ERKs), stress-activated protein kinases (SAPKs)/c-Jun NH2-terminal kinases (JNKs), and p38 MAPKs (p38). This is clinically relevant, because these pathways may be a possible target for anti-inflammatory drug intervention. This review studies the role of MAPKs in trauma and/or I/R.
Key concepts: p38 mitogen-activated protein kinases, Kinase, Mitogen-activated protein kinase, Medicine, Signal transduction, Ischemia, Inflammatory response, MAPK/ERK pathway