Charles Nicholas Serhan is the Simon Gelman Professor of Anaesthesia (Biochemistry and Molecular Pharmacology) at Harvard Medical School and a professor of Oral Medicine, Infection and Immunity at Harvard School of Dental Medicine. [1] Serhan is the Director of the Center for Experimental Therapeutics and Reperfusion Injury at Brigham and Women's Hospital. [1]
Serhan completed his Bachelor of Science in biochemistry at State University of New York at Stony Brook in 1978. [2] In 1982, Serhan earned a doctorate in Experimental Pathology and Medical Sciences from New York University School of Medicine. [2] Following his graduation, Serhan began a postdoctoral fellowship at the Karolinska Institute in Stockholm, Sweden under the mentorship of Bengt Samuelsson. [3] Serhan has also received honorary degrees from Harvard University, [1] University College Dublin, [4] and Queen Mary College, University of London. [5]
The focus of Serhan's research are Specialized Pro-Resolving Mediators (SPMs), which are "inflammation-fighting molecules in the body derived from essential fatty acids". [6] While working with Mats Hamberg and Bengt Samuelsson at the Karolinska Institute, Serhan helped discover lipoxin [7] the first of the SPMs to be elucidated. [8] Since this initial discovery, Serhan has identified additional mediators including Resolvins, Maresins, and Protectins. [9]
Serhan became a faculty member at Harvard Medical School in 1987 [3] and the Director of the Center for Experimental Therapeutics and Reperfusion Injury at Brigham and Women's Hospital (CET&RI). [1] The CET&RI's mission is: "To identify novel mediators, pathways, and their cellular receptors and targets critical in promoting resolution of inflammation and reperfusion tissue injury and establish their relation to human disease". [10]
Serhan was awarded the John Vane Medal from The William Harvey Research Institute in 2008. [11] In 2016, he received the Ross Prize in Molecular Medicine. [12] He was awarded the International Eicosanoid Research Foundation's 2017 Lifetime Achievement Award. [13] Serhan was the American Society for Investigative Pathology (ASIP) Rous-Whipple Award recipient in 2018 [14] and became an Honorary Life Member of the Society for Leukocyte Biology in 2019. [15] In 2022, Serhan delivered the Hans L. Falk Memorial Lecture at the National Institute of Environmental Health Sciences. [16]
The Karolinska Institute is a research-led medical university in Solna within the Stockholm urban area of Sweden and one of the foremost medical research institutes globally. The Nobel Assembly at the Karolinska Institute awards the Nobel Prize in Physiology or Medicine. The assembly consists of fifty professors from various medical disciplines at the university. The current vice-chancellor of Karolinska Institute is Annika Östman Wernerson, who took office in March 2023.
Arachidonic acid is a polyunsaturated omega-6 fatty acid 20:4(ω-6), or 20:4(5,8,11,14). If its precursors or diet contains linoleic acid it is formed by biosynthesis and can be deposited in animal fats. It is a precursor in the formation of leukotrienes, prostaglandins, and thromboxanes.
Bengt Ingemar Samuelsson was a Swedish biochemist. He shared with Sune K. Bergström and John R. Vane the 1982 Nobel Prize for Physiology or Medicine for discoveries concerning prostaglandins and related substances.
Eicosanoids are signaling molecules made by the enzymatic or non-enzymatic oxidation of arachidonic acid or other polyunsaturated fatty acids (PUFAs) that are, similar to arachidonic acid, around 20 carbon units in length. Eicosanoids are a sub-category of oxylipins, i.e. oxidized fatty acids of diverse carbon units in length, and are distinguished from other oxylipins by their overwhelming importance as cell signaling molecules. Eicosanoids function in diverse physiological systems and pathological processes such as: mounting or inhibiting inflammation, allergy, fever and other immune responses; regulating the abortion of pregnancy and normal childbirth; contributing to the perception of pain; regulating cell growth; controlling blood pressure; and modulating the regional flow of blood to tissues. In performing these roles, eicosanoids most often act as autocrine signaling agents to impact their cells of origin or as paracrine signaling agents to impact cells in the proximity of their cells of origin. Some eicosanoids, such as prostaglandins, may also have endocrine roles as hormones to influence the function of distant cells.
A lipoxin (LX or Lx), an acronym for lipoxygenase interaction product, is a bioactive autacoid metabolite of arachidonic acid made by various cell types. They are categorized as nonclassic eicosanoids and members of the specialized pro-resolving mediators (SPMs) family of polyunsaturated fatty acid (PUFA) metabolites. Like other SPMs, LXs form during, and then act to resolve, inflammatory responses. Initially, two lipoxins were identified, lipoxin A4 (LXA4) and LXB4, but more recent studies have identified epimers of these two LXs: the epi-lipoxins, 15-epi-LXA4 and 15-epi-LXB4 respectively.
Sir Salvador Enrique Moncada Seidner, FRS, FRCP, FMedSci is a Honduran-British pharmacologist and professor. He is currently Research Domain Director for Cancer at the University of Manchester.
Most of the eicosanoid receptors are integral membrane protein G protein-coupled receptors (GPCRs) that bind and respond to eicosanoid signaling molecules. Eicosanoids are rapidly metabolized to inactive products and therefore are short-lived. Accordingly, the eicosanoid-receptor interaction is typically limited to a local interaction: cells, upon stimulation, metabolize arachidonic acid to an eicosanoid which then binds cognate receptors on either its parent cell or on nearby cells to trigger functional responses within a restricted tissue area, e.g. an inflammatory response to an invading pathogen. In some cases, however, the synthesized eicosanoid travels through the blood to trigger systemic or coordinated tissue responses, e.g. prostaglandin (PG) E2 released locally travels to the hypothalamus to trigger a febrile reaction. An example of a non-GPCR receptor that binds many eicosanoids is the PPAR-γ nuclear receptor.
Leukotriene A4 (LTA4) is a leukotriene, and is the precursor for the productions of leukotriene B4 (LTB4) and leukotriene C4 (LTC4).
ALOX15 is, like other lipoxygenases, a seminal enzyme in the metabolism of polyunsaturated fatty acids to a wide range of physiologically and pathologically important products. ▼ Gene Function
ALOX12, also known as arachidonate 12-lipoxygenase, 12-lipoxygenase, 12S-Lipoxygenase, 12-LOX, and 12S-LOX is a lipoxygenase-type enzyme that in humans is encoded by the ALOX12 gene which is located along with other lipoyxgenases on chromosome 17p13.3. ALOX12 is 75 kilodalton protein composed of 663 amino acids.
N-formyl peptide receptor 2 (FPR2) is a G-protein coupled receptor (GPCR) located on the surface of many cell types of various animal species. The human receptor protein is encoded by the FPR2 gene and is activated to regulate cell function by binding any one of a wide variety of ligands including not only certain N-Formylmethionine-containing oligopeptides such as N-Formylmethionine-leucyl-phenylalanine (FMLP) but also the polyunsaturated fatty acid metabolite of arachidonic acid, lipoxin A4 (LXA4). Because of its interaction with lipoxin A4, FPR2 is also commonly named the ALX/FPR2 or just ALX receptor.
Cyclooxygenase 1 (COX-1), also known as prostaglandin-endoperoxide synthase 1, is an enzyme that in humans is encoded by the PTGS1 gene. In humans it is one of two cyclooxygenases.
G protein-coupled receptor 32, also known as GPR32 or the RvD1 receptor, is a human receptor (biochemistry) belonging to the rhodopsin-like subfamily of G protein-coupled receptors.
Kevin J. Tracey, a neurosurgeon and inventor, is the president and CEO of the Feinstein Institute for Medical Research, professor of neurosurgery and molecular medicine at the Zucker School of Medicine, and president of the Elmezzi Graduate School of Molecular Medicine in Manhasset, New York. The Public Library of Science Magazine, PLOS Biology, recognized Tracey in 2019 as one of the most cited researchers in the world.
Göran K. Hansson, is a Swedish physician and scientist.
Maresin 1 (MaR1 or 7R,14S-dihydroxy-4Z,8E,10E,12Z,16Z,19Z-docosahexaenoic acid) is a macrophage-derived mediator of inflammation resolution coined from macrophage mediator in resolving inflammation. Maresin 1, and more recently defined maresins, are 12-lipoxygenase-derived metabolites of the omega-3 fatty acid, docosahexaenoic acid (DHA), that possess potent anti-inflammatory, pro-resolving, protective, and pro-healing properties similar to a variety of other members of the specialized proresolving mediators (SPM) class of polyunsaturated fatty acid (PUFA) metabolites. SPM are dihydroxy, trihydroxy, and epoxy-hydroxy metabolites of long chain PUFA made by certain dioxygenase enzymes viz., cyclooxygenases and lipoxygenases. In addition to the maresins, this class of mediators includes: the 15-lipoxygenase (i.e. ALOX15 and/or possibly ALOX15B)-derived lipoxin A4 and B4 metabolites of the omega 6 fatty acid, arachidonic acid; the cyclooxygenase 2-derived resolvin E series metabolites of the omega 3 fatty acid, eicosapentaenoic acid; certain 15-lipoxygenase-derived resolvin D series metabolites of DHA; certain other 15-lipoxygenase-derived protectin D1 and related metabolites of DHA; and the more recently defined and therefore less fully studied 15-lipoxygenase-derived resolvin Dn-3DPA metabolites of the omega-3 fatty acid n-3 docosapentaenoic acid (n-3 DPA or clupanodonic acid), the cyclooxygenase 2-derived resolvin T metabolites of this clupanodonic acid, and the 15-lipoxygenase-derived products of the N-acetylated fatty acid amide of the DHA metabolite, docosahexaenoyl ethanolamide.
Specialized pro-resolving mediators are a large and growing class of cell signaling molecules formed in cells by the metabolism of polyunsaturated fatty acids (PUFA) by one or a combination of lipoxygenase, cyclooxygenase, and cytochrome P450 monooxygenase enzymes. Pre-clinical studies, primarily in animal models and human tissues, implicate SPM in orchestrating the resolution of inflammation. Prominent members include the resolvins and protectins.
Ramzi S. Cotran (1932-2000) was a pathologist and former president of the United States and Canadian Academy of Pathology (USCAP) and the American Society for Investigative Pathology (ASIP). He was chair of pathology at Harvard's Brigham and Women's Hospital and Children's Hospital Medical Center, as well as the Frank B. Mallory Professor of Pathology at Harvard Medical School and a member of the National Academy of Science's Institute of Medicine. The Ramzi Cotran Young Investigator Award is presented each year by USCAP to a pathologist in recognition of a body of investigative work which has contributed significantly to the diagnosis and understanding of human disease. The ASIP Cotran Early Career Investigator Award is presented each year by ASIP, and recognizes early career investigators who direct independent experimental pathology research programs that are focused on improvement of the understanding of the conceptual basis of disease.
Vijay K. Kuchroo is an Indian-American immunologist and serial entrepreneur. He is the Samuel L. Wasserstrom chair of Neurology at Harvard Medical School, and Brigham and Women's Hospital. He is also the director of the Evergrande Center for Immunologic Diseases at Harvard Medical School and Brigham and Women's Hospital in Boston, Massachusetts.
Dennis L. Kasper is an American microbiologist and immunologist, and the William Ellery Channing Professor of Medicine and Professor of Immunology at Harvard Medical School. He leads the Kasper Laboratory within the Blavatnik Institute in the Department of Immunology at Harvard Medical School. He was also executive dean for academic programs at Harvard Medical School and director of the Channing Laboratory Department of Medicine at Brigham and Women's Hospital.