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Calcium,mitochondria and the initiation of acute pancreatitis
Affiliation:1. Division of Digestive and Liver Diseases, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA;2. Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA;1. Nutrition Services, Royal North Shore Hospital, St. Leonards, NSW, Australia;2. Sydney Vital, Sydney, NSW, Australia;3. Upper GI Surgical Unit, Royal North Shore Hospital, St. Leonards, NSW, Australia;4. Northern Clinical School, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia;5. Department of Biochemistry, Royal North Shore Hospital, St. Leonards, NSW, Australia;6. Department of Medical Oncology, Royal North Shore Hospital, St. Leonards, NSW, Australia;7. Department of Endocrinology, Royal North Shore Hospital, St. Leonards, NSW, Australia;8. NSW Health Pathology, Macquarie University, North Ryde, NSW, Australia;9. Australian Pancreatic Centre, Sydney, NSW, Australia;10. Cancer Diagnosis and Pathology Group, Kolling Institute, The University of Sydney, Australia;11. University of Notre Dame Australia, Australia;1. Department of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA;2. Department of Radiology, Massachusetts General Hospital, Boston, MA, USA;1. Department of Pancreatic Surgery, General Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, China;2. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, China;3. Department of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, China;1. The Health and Rehabilitation Research Institute, School of Clinical Sciences, Faculty of Health and Environmental Sciences, Auckland University of Technology (AUT), Auckland, New Zealand;2. The Auckland Regional Pain Service (TARPS), Auckland District Health Board (ADHB), Auckland, New Zealand;3. The Pain Management Unit, Department of Anaesthesia and Perioperative Medicine, Waitematā District Health Board (WDHB), Auckland, New Zealand;4. Department of Surgery, School of Medicine, Faculty of Medical and Health Science, University of Auckland, New Zealand;5. Centre for Pancreatic Diseases & Mech-Sense, Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark;6. Department of Internal Medicine, Randers Regional Hospital, Randers, Denmark;7. Department of Clinical Medicine, Aalborg University, Aalborg, Denmark;8. Department of Psychological Medicine, Faculty of Medical and Health Science, University of Auckland, New Zealand;9. Department of General Surgery, Counties Manukau District Health Board (CMDHB), Auckland, New Zealand;1. Division of Gastroenterology, Hepatology and Nutrition, University of Minnesota, USA;2. Department of Radiology, University of Minnesota, USA;3. Clinical and Translational Science Institute, Biostatistical Design and Analysis Center, University of Minnesota, USA;1. Indiana University School of Medicine, United States;2. Charles Warren Fairbanks Center of Medical Ethics, Indiana University Health, United States;3. Lehman, Bucksot and Sherman Section of Pancreatobiliary Endoscopy, United States
Abstract:Acute pancreatitis is characterized by necrosis of its parenchymal cells and influx and activation of inflammatory cells that further promote injury and necrosis. This review is intended to discuss the central role of disorders of calcium metabolism and mitochondrial dysfunction in the mechanism of pancreatitis development. The disorders are placed in context of calcium and mitochondria in physiologic function of the pancreas. Moreover, we discuss potential therapeutics for preventing pathologic calcium signals that injure mitochondria and interventions that promote the removal of injured mitochondria and regenerate new and heathy populations of mitochondria.
Keywords:Acute pancreatitis  Calcium  Mitochondria  Necrosis  Inflammation  Autophagy  Mitophagy
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