腺泡细胞钙离子超载与急性胰腺炎关系的研究进展

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Abstract Acute pancreatitis (AP) is one of the most common diseases in the department of gastroenterology. Most patients are mild, but about 25% of patients develop severe pancreatitis, and the fatality rate of severe pancreatitis is as high as 30%-50%. Domestic, according to a lot of basic research on the etiology and pathogenesis of AP use hyla element method, induction method, bravery, no bile salts b methionine food pancreatic duct retrograde bezoar AP animal models induced by bile acid sodium injection acini intracellular calcium ion concentration are rising, resulting in intracellular calcium dependent enzyme activation and cavitation in advance of the original particles into ultimately lead to cell apoptosis, the above conclusions are prompted acinar cell calcium overload play a crucial role in the occurence and development of AP, and treatment for the AP is lack of efficient and clinical targeted drugs targeted, so the exploring to maintain the mechanism of intracellular calcium homeostasis and acinar cells of the pathological process of calcium overload caused by, for the research of the AP directly targeted drugs provide a new way of thinking. In this review, intracellular calcium homeostasis and regulation, calcium overload in acinar cells, the role of Ca2+ overload in the pathogenesis of AP, and the clinical diagnosis and treatment of Ca2+ overload in acinar cells are reviewed.

Key words： Acute pancreatitis Calcium overload Acinar cell Treatment Review

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	YANG Jingjing GAO Xiang

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YANG Jingjing GAO Xiang. Research progress on the relationship between calcium overload in acinar cells and acute pancreatitis[J]. 中国当代医药, 2024, 31(1): 192-198.

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https://www.dangdaiyiyao.com/EN/ OR https://www.dangdaiyiyao.com/EN/Y2024/V31/I1/192

[1]	Liu LW，Xie Y，Li GQ，et al.Gut microbiota-derived nicotinamide mononucleotide alleviates acute pancreatitis by activating pancreatic SIRT3 signalling[J].Br J Pharmacol，2023， 180（5）：647-666.
[2]	Feng S，Wei Q，Hu Q，et al.Research progress on the relationship between acute pancreatitis and calcium overload in acinar cells[J].Dig Dis Sci，2019，64（1）：25-38.
[3]	Gerasimenko OV，Gerasimenko JV.CRAC channel inhibitors in pancreatic pathologies[J].J Physiol，2022，600（7）：1597.
[4]	Romero-Garcia S，Prado-Garcia H.Mitochondrial calcium：Transport and modulation of cellular processes in homeostasis and cancer[J].Int J Oncol，2019，54（4）：1155-1167.
[5]	Zhao H，Li Z，Liu Y，et al.Mitochondrial Calcium Homeostasis in the Pathology and Therapeutic Application in Friedreich's Ataxia[J].Neurosci Bull，2023，39（4）：695-698.
[6]	Groenendyk J，Agellon LB，Michalak M.Calcium signaling and endoplasmic reticulum stress[J].Int Rev Cell Mol Biol，2021， 363：1-20.
[7]	Malek M，Wawrzyniak AM，Koch P，et al.Inositol triphosphate-triggered calcium release blocks lipid exchange at endoplasmic reticulum-Golgi contact sites[J].Nat Commun，2021，12（1）：1-16.
[8]	Lakananurak N，Gramlich L.Nutrition management in acute pancreatitis：Clinical practice consideration[J].World J Clin Cases，2020，8（9）：1561.
[9]	牛梦亚，文礼.病理性钙信号与急性胰腺炎[J].中华胰腺病杂志，2022，22（1）：22-29.
[10]	Belosludtsev KN，Dubinin MV，Belosludtseva NV，et al.Mitochondrial Ca2+ Transport：Mechanisms，Molecular Structures，and Role in Cells[J].Biochemistry (Mosc)，2019，84（6）：593-607.
[11]	Carreras-Sureda A，Pihán P，Hetz C.Calcium signaling at the endoplasmic reticulum：fine-tuning stress responses[J].Cell Calcium，2018，70：24-31.
[12]	Gil D，Diercks BP，Guse AH，et al.Three-Dimensional Model of Sub-Plasmalemmal Ca2+ Microdomains Evoked by T Cell Receptor/CD3 Complex Stimulation[J].Front Mol Biosci，2022，9：811145.
[13]	Rodríguez-Prados M，Rojo-Ruiz J，García-Sancho J，et al.Direct monitoring of ER Ca2+ dynamics reveals that Ca2+entry induces ER-Ca2+ release in astrocytes[J].Pflugers Arch，2020，472（4）：439-448.
[14]	Liau NPD，Laktyushin A，Lucet IS，et al.The molecular basis of JAK/STAT inhibition by SOCS1[J].Nat Commun，2018，9（1）：1-14.
[15]	Bettaieb L，Brulé M，Chomy A，et al.Ca2+ Signaling and Its Potential Targeting in Pancreatic Ductal Carcinoma[J].Cancers，2021，13（12）：3085.
[16]	Wang G，Zhang J，Xu C，et al.Inhibition of SOCs attenuates acute lung injury induced by severe acute pancreatitis in rats and PMVECs injury induced by lipopolysaccharide[J].Inflammation，2016，39（3）：1049-1058.
[17]	Hu G，Peng C，Xie X，et al.Patchouli alcohol isolated from Pogostemon cablin mediates endothelium-independent vasorelaxation by blockade of Ca2+ channels in rat isolated thoracic aorta[J].J Ethnopharmacol，2018，220：188-196.
[18]	Hofschr■er V，Najder K，Rugi M，et al.Ion channels orchestrate pancreatic ductal adenocarcinoma progression and therapy[J].Front Pharmacol，2021，11：586599.
[19]	Rosenbaum T，Benítez-Angeles M，Sánchez-Hernández R，et al.TRPV4：a physio and pathophysiologically significant ion channel[J].Int J Mol Sci，2020，21（11）：3837.
[20]	Swain SM，Romac JMJ，Shahid RA，et al.TRPV4 channel opening mediates pressure-induced pancreatitis initiated by Piezo1 activation[J].J Clin Invest，2020，130（5）：2527-2541.
[21]	Wagner J，Keizer J.Effects of rapid buffers on Ca2+ diffusion and Ca2+oscillations[J]. Biophys J，1994，67（1）：447-456.
[22]	Serafini M，Cordero-Sanchez C，Di Paola R，et al.Store-operated calcium entry as a therapeutic target in acute pancreatitis：discovery and development of drug-like SOCE inhibitors[J].J Med Chem，2020，63（23）：14761-14779.
[23]	Gilabert JA.Cytoplasmic calcium buffering：an integrative crosstalk[J].Adv Exp Med Biol，2020，1131：163-182.
[24]	Gutiérrez LG，Hernández-Morales M，Núnez L，et al.Inhibition of polyamine biosynthesis reverses Ca2+ channel remodeling in colon cancer cells[J].Cancers，2019，11（1）：83.
[25]	杨晶晶，陈嘉屿.肠道微生物失衡在慢性便秘中作用的研究进展[J].基础医学与临床，2021，41（04）：593-597.
[26]	Sluga N，Posti■ S，Sarikas S，et al.Dual mode of action of acetylcholine on cytosolic calcium oscillations in pancreatic beta and acinar cells in situ[J].Cells，2021，10（7）：1580.
[27]	Félix-Martínez GJ，González-Vélez V，Godínez-Fernández JR，et al.Electrophysiological models of the human pancreaticδ-cell：From single channels to the firing of action potentials[J]. Int J Numer Method Biomed Eng，2020，36（2）：e3296.27.
[28]	吴嘉麒，刘鑫，王宁，等.抑制内质网钙离子释放在诱导巨噬细胞自噬及逆转LPS耐受中的作用[J].免疫学杂志，2020，36（1）：11-16.
[29]	Bruce JIE，Elliott AC.Oxidant-impaired intracellular Ca2+ signaling in pancreatic acinar cells：role of the plasma membrane Ca2+ -ATPase[J].Am J Physiol Cell Physiol，2007， 293（3）：C938-C950.
[30]	Novickij V，Rembialkowska N，Staigvila G，et al.Effects of extracellular medium conductivity on cell response in the context of sub-microsecond range calcium electroporation[J].Sci Rep，2020，10（1）：1-12.
[31]	Park Y，Ku L，Lim JW，et al.Docosahexaenoic acid inhibits zymogen activation by suppressing vacuolar ATPase activation in cerulein-stimulated pancreatic acinar cells[J].Genes Nutr，2020，15（1）：1-10.
[32]	Hirota M，Ohmuraya M，Hashimoto D，et al.Roles of autophagy and pancreatic secretory trypsin inhibitor in trypsinogen activation in acute pancreatitis[J].Pancreas，2020，49（4）：493-497.
[33]	Kolodecik TR，Reed AM，Date K，et al.The serum protein renalase reduces injury in experimental pancreatitis[J]. J Biol Chem，2017，292（51）：21047-21059.
[34]	Cui TY，Liu RX，Yin CG.Research advances in abnormal activation and secretion of pancreatic enzymes in acute pancreatitis[J].J Clin Hepatol，2022，38（5）：1198-1202.
[35]	Chen W，Yuan C，Lu Y，et al.Tanshinone IIA Protects against Acute Pancreatitis in Mice by Inhibiting Oxidative Stress via the Nrf2/ROS Pathway[J].Oxid Med Cell Longev，2020，2020（5）：1-12.
[36]	吴英珂，王卫星.线粒体损伤在急性胰腺炎发病机制中的作用[J].中国普通外科杂，2020，29（9）：1141-1146.
[37]	Dur A，Kocaman O，Kocyigit A，et al.Oxidative status and lymphocyte DNA damage in patients with acute pancreatitis and its relationship with severity of acute pancreatitis[J].Turk J Gastroenterol，2016，27（1）：68.
[38]	Mayerle J，Sendler M，Hegyi E，et al.Genetics and Pathophysiology of Pancreatitis[J].Gastroenterology，2019，156（7）：1951-1968.
[39]	Petersen OH，Gerasimenko JV，Gerasimenko OV，et al.The roles of calcium and ATP in the physiology and pathology of the exocrine pancreas[J].Physiol Rev，2021，101（4）：1691- 1744.
[40]	Manhas N，Anbazhagan N.A mathematical model of intricate calcium dynamics and modulation of calcium signalling by mitochondria in pancreatic acinar cells[J].Chaos Solitons Fractals，2021，145：110741.
[41]	Stozer A，Dolensek J，Bombek LK，et al.Confocal laser scanning microscopy of calcium dynamics in acute mouse pancreatic tissue slices[J].J Vis Exp，2021（170）：e62293.
[42]	Demine S，Renard P，Arnould T.Mitochondrial uncoupling：a key controller of biological processes in physiology and diseases[J].Cells，2019，8（8）：795.
[43]	Bonora M，Giorgi C，Pinton P.Molecular mechanisms and consequences of mitochondrial permeability transition[J].Nat Rev Mol Cell Biol，2022，23（4）：266-285.
[44]	Bruce JIE，Sánchez-Alvarez R，Sans MD，et al.Insulin protects acinar cells during pancreatitis by preserving glycolytic ATP supply to calcium pumps[J].Nat Commun，2021，12（1）：4386.
[45]	Pallagi P，G■r■g M，Papp N，et al.Bile acid-and ethanol‐mediated activation of Orai1 damages pancreatic ductal secretion in acute pancreatitis[J].J Physiol，2022，600（7）：1631-1650.
[46]	Bruen C，Miller J，Wilburn J，et al.Auxora for the treatment of patients with acute pancreatitis and accompanying systemic inflammatory response syndrome：clinical development of a calcium release-activated calcium channel inhibitor[J].Pancreas，2021，50（4）：537.
[47]	Fanczal J，Pallagi P，G■r■g M，et al.TRPM2-mediated extracellular Ca2+ entry promotes acinar cell necrosis in biliary acute pancreatitis[J].J Physiol，2020，598（6）：1253-1270.
[48]	Yuan J，Wei Z，Xin G，et al.Vitamin B12 Attenuates Acute Pancreatitis by Suppressing Oxidative Stress and Improving Mitochondria Dysfunction via CBS/SIRT1 Pathway[J].Oxid Med Cell Longev，2021：7936316.
[49]	Yu X，Dai C，Zhao X，et al.Ruthenium red attenuates acute pancreatitis by inhibiting MCU and improving mitochondrial function[J].Biochem Biophys Res Commun，2022，635：236- 243.