Please wait a minute...
J Zhejiang Univ (Med Sci)  2021, Vol. 50 Issue (2): 267-276    DOI: 10.3724/zdxbyxb-2021-0110
    
Research progress on transient receptor potential melastatin 2 channel in nervous system diseases
YING Yingchao(),JIANG Peifang()
Department of Neurology, the Children’s Hospital, Zhejiang University School of Medicine, Hangzhou 310052, China
Download: HTML( 11 )   PDF(3560KB)
Export: BibTeX | EndNote (RIS)      

Abstract  

Transient receptor potential M2 (TRPM2) ion channel is a non-selective cationic channel that can permeate calcium ions, and plays an important role in neuroinflammation, ischemic reperfusion brain injury, neurodegenerative disease, neuropathic pain, epilepsy and other neurological diseases. In ischemic reperfusion brain injury, TRPM2 mediates neuronal death by modulating the different subunits of glutamate N-methyl-D-aspartic acid receptor in response to calcium/zinc signal. In Alzheimer’s disease, TRPM2 is activated by reactive oxygen species generated by β-amyloid peptide to form a malignant positive feedback loop that induces neuronal death and is involved in the pathological process of glial cells by promoting inflammatory response and oxidative stress. In epilepsy, the TRPM2-knockout alleviates epilepsy induced neuronal degeneration by inhibiting autophagy and apoptosis related proteins. The roles of TRPM2 channel in the pathogenesis of various central nervous system diseases and its potential drug development and clinical application prospects are summarized in this review.



Key wordsTransient receptor potential melastain 2      Nervous system diseases      Ischemia-reperfusion brain injury      Alzheimer’s disease      Epilepsy      Juvenile myoclonic epilepsy      Review     
Received: 15 October 2020      Published: 18 June 2021
CLC:  R741  
Corresponding Authors: JIANG Peifang     E-mail: yyc123@zju.edu.cn;jiangpeifang@zju.edu.cn
Cite this article:

YING Yingchao,JIANG Peifang. Research progress on transient receptor potential melastatin 2 channel in nervous system diseases. J Zhejiang Univ (Med Sci), 2021, 50(2): 267-276.

URL:

http://www.zjujournals.com/med/10.3724/zdxbyxb-2021-0110     OR     http://www.zjujournals.com/med/Y2021/V50/I2/267


瞬时受体电位 M2 型离子通道在神经系统疾病中的作用研究进展

瞬时受体电位 M2 型(TRPM2)离子通道是可渗透钙离子的非选择性阳离子通道,在神经炎症、缺血再灌注脑损伤、神经退行性病变、神经病理性疼痛、癫痫等多种神经系统疾病中发挥重要作用。在缺血再灌注脑损伤中,TRPM2 通过调节谷氨酸离子 N-甲基-D-天冬氨酸受体不同亚基、响应钙离子/锌离子信号,介导神经元死亡。在阿尔茨海默病中,TRPM2 被β-淀粉样肽生成的活性氧激活形成恶性正反馈循环诱导神经元死亡,并在胶质细胞中通过促进炎症反应和氧化应激参与其病理过程。在癫痫中,TRPM2 基因敲除通过抑制自噬和凋亡相关蛋白,减轻癫痫引起的神经元变性。本文总结了近年来 TRPM2 通道在多种中枢神经系统疾病发病机制中的作用及其潜在的药物研发和临床应用前景。


关键词: 瞬时受体电位 M2 型,  神经系统疾病,  缺血再灌注脑损伤,  阿尔茨海默病,  癫痫,  青少年肌阵挛癫痫,  综述 
Figure 1 The mechanism of NMDAR-related TRPM2 channels mediating ischemic reperfusion brain injury
Figure 2 Common mechanisms of neuronal death induced by TRPM2 in different types of neurological diseases
[1]   MALKOP, SYED MORTADZAS A, MCWILLIAMJ, et al.TRPM2 channel in microglia as a new player in neuroinflammation associated with a spectrum of central nervous system pathologies[J]Front pharmacol, 2019, 239.
doi: 10.3389/fphar.2019.00239
[2]   XIEY F, BELROSEJ C, LEIG, et al.Dependence of NMDA/GSK-3β mediated metaplasticity on TRPM2 channels at hippocampal CA3-CA1 synapses[J]Mol Brain, 2011, 4( 1): 44.
doi: 10.1186/1756-6606-4-44
[3]   JANGY, LEES H, LEEB, et al.TRPM2, a susceptibility gene for bipolar disorder, regulates glycogen synthase kinase-3 activity in the brain[J]J Neurosci, 2015, 35( 34): 11811-11823.
doi: 10.1523/JNEUROSCI.5251-14.2015
[4]   BAIJ Z, LIPSKIJ. Differential expression of TRPM2 and TRPV4 channels and their potential role in oxidative stress-induced cell death in organotypic hippocampal culture[J]NeuroToxicology, 2010, 31( 2): 204-214.
doi: 10.1016/j.neuro.2010.01.001
[5]   BELROSEJ C, XIEY F, GIERSZEWSKIL J, et al.Loss of glutathione homeostasis associated with neuronal senescence facilitates TRPM2 channel activation in cultured hippocampal pyramidal neurons[J]Mol Brain, 2012, 5( 1): 11.
doi: 10.1186/1756-6606-5-11
[6]   LIX, JIANGL H. Multiple molecular mechanisms form a positive feedback loop driving amyloid β42 peptide-induced neurotoxicity via activation of the TRPM2 channel in hippocampal neurons[J]Cell Death Dis, 2018, 9( 2): 195.
doi: 10.1038/s41419-018-0270-1
[7]   KANEKOS, KAWAKAMIS, HARAY, et al.A critical role of TRPM2 in neuronal cell death by hydrogen peroxide[J]J Pharmacol Sci, 2006, 101( 1): 66-76.
doi: 10.1254/jphs.fp0060128
[8]   HILLK, TIGUEN J, KELSELLR E, et al.Characterisation of recombinant rat TRPM2 and a TRPM2-like conductance in cultured rat striatal neurones[J]Neuropharmacology, 2006, 50( 1): 89-97.
doi: 10.1016/j.neuropharm.2005.08.021
[9]   SUNY, SUKUMARANP, SELVARAJS, et al.TRPM2 and a TRPM2-like conductance in cultured rat striatal neurones[J]l, 2018, 55( 1): 409-420.
doi: 10.1007/s12035-016-0338-9
[10]   CHUNGK K H, FREESTONEP S, LIPSKIJ. Expression and functional properties of TRPM2 channels in dopaminergic neurons of the substantia nigra of the rat[J]J NeuroPhysiol, 2011, 106( 6): 2865-2875.
doi: 10.1152/jn.00994.2010
[11]   KRAFTR, GRIMMC, GROSSEK, et al.Hydrogen peroxide and ADP-ribose induce TRPM2-mediated calcium influx and cation currents in microglia[J]Am J Physiol-Cell Physiol, 2004, 286( 1): C129-C137.
doi: 10.1152/ajpcell.00331.2003
[12]   SMITHM A, HERSONP S, LEEK, et al.Hydrogen peroxide and ADP-ribose induce TRPM2-mediated calcium influx and cation currents in microglia[J]J Physiol, 2003, 547( 2): 417-425.
doi: 10.1113/jphysiol.2002.034561
[13]   JIANGL H, LIX, SYED MORTADZAS A, et al.The TRPM2 channel nexus from oxidative damage to Alzheimer’s pathologies: an emerging novel intervention target for age-related dementia[J]Ageing Res Rev, 2018, 67-79.
doi: 10.1016/j.arr.2018.07.002
[14]   OSTAPCHENKOV G, CHENM, GUZMANM S, et al.The transient receptor potential melastatin 2 (TRPM2) channel contributes to β-amyloid oligomer-related neurotoxicity and memory impairment[J]J Neurosci, 2015, 35( 45): 15157-15169.
doi: 10.1523/jneurosci.4081-14.2015
[15]   KOS Y, WANGS E, LEEH K, et al.Transient receptor potential melastatin 2 governs stress-induced depressive-like behaviors[J]Proc Natl Acad Sci U S A, 2019, 116( 5): 1770-1775.
doi: 10.1073/pnas.1814335116
[16]   KURINCZUKJ J, WHITE-KONINGM, BADAWIN. Epidemiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy[J]Early Hum Dev, 2010, 86( 6): 329-338.
doi: 10.1016/j.earlhumdev.2010.05.010
[17]   MILLARL J, SHIL, HOERDER-SUABEDISSENA, et al.Neonatal hypoxia ischaemia: mechanisms, models, and therapeutic challenges[J]Front Cell Neurosci, 2017, 78.
doi: 10.3389/fncel.2017.00078
[18]   JIAJ, VERMAS, NAKAYAMAS, et al.Sex differences in neuroprotection provided by inhibition of TRPM2 channels following experimental stroke[J]J Cereb Blood Flow Metab, 2011, 31( 11): 2160-2168.
doi: 10.1038/jcbfm.2011.77
[19]   VERMAS, QUILLINANN, YANGY F, et al.TRPM2 channel activation following in vitro ischemia contributes to male hippocampal cell death[J]NeuroSci Lett, 2012, 530( 1): 41-46.
doi: 10.1016/j.neulet.2012.09.044
[20]   SHIMIZUT, MACEYT A, QUILLINANN, et al.Androgen and PARP-1 regulation of TRPM2 channels after ischemic injury[J]J Cereb Blood Flow Metab, 2013, 33( 10): 1549-1555.
doi: 10.1038/jcbfm.2013.105
[21]   ALIMI, TEVESL, LIR, et al.Modulation of NMDAR subunit expression by TRPM2 channels regulates neuronal vulnerability to ischemic cell death[J]J Neurosci, 2013, 33( 44): 17264-17277.
doi: 10.1523/jneurosci.1729-13.2013
[22]   SYED MORTADZAS A, WANGL, LID, et al.TRPM2 channel-mediated ROS-sensitive Ca(2+) signaling mechanisms in immune cells[J]Front Immunol, 2015, 407.
doi: 10.3389/fimmu.2015.00407
[23]   YEM, YANGW, AINSCOUGHJ F, et al.TRPM2 channel deficiency prevents delayed cytosolic Zn2+ accumulation and CA1 pyramidal neuronal death after transient global ischemia[J/OL]Cell Death Dis, 2014, 5( 11): e1541.
doi: 10.1038/cddis.2014.494
[24]   ZHANK, YUP, LIUC, et al.Detrimental or beneficial: the role of TRPM2 in ischemia/reperfusion injury[J]Acta Pharmacol Sin, 2016, 37( 1): 4-12.
doi: 10.1038/aps.2015.141
[25]   LAIT W, ZHANGS, WANGY T. Excitotoxicity and stroke: identifying novel targets for neuroprotection[J]Prog NeuroBiol, 2014, 157-188.
doi: 10.1016/j.pneurobio.2013.11.006
[26]   MAIC, MANKOOH, WEIL, et al.TRPM2 channel: A novel target for alleviating ischaemia‐reperfusion, chronic cerebral hypo-perfusion and neonatal hypoxic‐ischaemic brain damage[J]J Cell Mol Med, 2020, 24( 1): 4-12.
doi: 10.1111/jcmm.14679
[27]   ELTZSCHIGH K, ECKLET. Ischemia and reperfusion—from mechanism to translation[J]Nat Med, 2011, 17( 11): 1391-1401.
doi: 10.1038/nm.2507
[28]   DIETZR M, CRUZ-TORRESI, ORFILAJ E, et al.Reversal of global ischemia-induced cognitive dysfunction by delayed inhibition of TRPM2 ion channels[J]Transl Stroke Res, 2020, 11( 2): 254-266.
doi: 10.1007/s12975-019-00712-z
[29]   LIX, YANGW, JIANGL H. Alteration in Intracellular Zn2+ homeostasis as a result of TRPM2 channel activation contributes to ROS-induced hippocampal neuronal death[J]Front Mol Neurosci, 2017, 414.
doi: 10.3389/fnmol.2017.00414
[30]   STORKC J, LIY V. Rising zinc: a significant cause of ischemic neuronal death in the CA1 region of rat hippocampus[J]J Cereb Blood Flow Metab, 2009, 29( 8): 1399-1408.
doi: 10.1038/jcbfm.2009.64
[31]   SHUTTLEWORTHC W, WEISSJ H. Zinc: new clues to diverse roles in brain ischemia[J]Trends Pharmacol Sci, 2011, 32( 8): 480-486.
doi: 10.1016/j.tips.2011.04.001
[32]   LIX, JIANGL H. A critical role of the transient receptor potential melastatin 2 channel in a positive feedback mechanism for reactive oxygen species-induced delayed cell death[J]J Cell Physiol, 2019, 234( 4): 3647-3660.
doi: 10.1002/jcp.27134
[33]   ERKKINENM G, KIMM O, GESCHWINDM D. Clinical neurology and epidemiology of the major neurodegenerative diseases[J]Cold Spring Harb Perspect Biol, 2018, 10( 4): a033118.
doi: 10.1101/cshperspect.a033118
[34]   HASHIMOTOM, ROCKENSTEINE, CREWSL, et al.Role of protein aggregation in mitochondrial dysfunction and neurodegeneration in Alzheimer’s and Parkinson’s diseases[J]Neuromolecular Med, 2003, 4( 1-2): 21-36.
doi: 10.1385/nmm:4:1-2:21
[35]   TIRABOSCHIP, HANSENL A, THALL J, et al.The importance of neuritic plaques and tangles to the development and evolution of AD[J]Neurology, 2004, 62( 11): 1984-1989.
doi: 10.1212/01.wnl.0000129697.01779.0a
[36]   BOURASC, HOFP R, GIANNAKOPOULOSP, et al.Regional distribution of neurofibrillary tangles and senile plaques in the cerebral cortex of elderly patients: a quantitative evaluation of a one-year autopsy population from a geriatric hospital[J]Cereb Cortex, 1994, 4( 2): 138-150.
doi: 10.1093/cercor/4.2.138
[37]   BACHURINS O, BOVINAE V, USTYUGOVA A. Drugs in clinical trials for Alzheimer’s disease: the major trends[J]Med Res Rev, 2017, 37( 5): 1186-1225.
doi: 10.1002/med.21434
[38]   BLENNOWK, ZETTERBERGH. Biomarkers for Alzheimer’s disease: current status and prospects for the future[J]J Intern Med, 2018, 284( 6): 643-663.
doi: 10.1111/joim.12816
[39]   SELKOED J, HARDYJ. The amyloid hypothesis of Alzheimer’s disease at 25 years[J]EMBO Mol Med, 2016, 8( 6): 595-608.
doi: 10.15252/emmm.201606210
[40]   JANKOWSKYJ L, XUG, FROMHOLTD, et al.Environmental enrichment exacerbates amyloid plaque formation in a transgenic mouse model of Alzheimer disease[J]l, 2003, 62( 12): 1220-1227.
doi: 10.1093/jnen/62.12.1220
[41]   DE FELICEF G, VELASCOP T, LAMBERTM P, et al.Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine[J]J Biol Chem, 2007, 282( 15): 11590-11601.
doi: 10.1074/jbc.M607483200
[42]   LAFERLAF M. Calcium dyshomeostasis and intracellular signalling in Alzheimer’s disease[J]Nat Rev Neurosci, 2002, 3( 11): 862-872.
doi: 10.1038/nrn960
[43]   OLAHM E, JACKSONM F, LIH, et al.Ca2+-dependent induction of TRPM2 currents in hippocampal neurons[J]J Physiol, 2009, 587( 5): 965-979.
doi: 10.1113/jphysiol.2008.162289
[44]   ?VEY? S, NAZ?RO?LUM. Effects of homocysteine and memantine on oxidative stress related TRP cation channels in in-vitro model of Alzheimer’s disease[J]J Receptor Signal Transduct, 2021, 41( 3): 273-283.
doi: 10.1080/10799893.2020.1806321
[45]   REGENF, HELLMANN-REGENJ, COSTANTINIE, et al.Neuroinflammation and Alzheimer’s disease: implications for microglial activation[J]Curr Alzheimer Res, 2017, 14( 11): 1140-1148.
doi: 10.2174/1567205014666170203141717
[46]   AHMADM H, FATIMAM, MONDALA C. Influence of microglia and astrocyte activation in the neuroinflammatory pathogenesis of Alzheimer’s disease: Rational insights for the therapeutic approaches[J]J Clin Neurosci, 2019, 6-11.
doi: 10.1016/j.jocn.2018.10.034
[47]   WANGJ, JACKSONM F, XIEY F. Glia and TRPM2 channels in plasticity of central nervous system and Alzheimer’s diseases[J]Neural Plast, 2016, 168-0905.
doi: 10.1155/2016/1680905
[48]   LEEM, CHOT, JANTARATNOTAIN, et al.Depletion of GSH in glial cells induces neurotoxicity: relevance to aging and degenerative neurological diseases[J]FASEB J, 2010, 24( 7): 2533-2545.
doi: 10.1096/fj.09-149997
[49]   SAHARANS, MANDALP K. The emerging role of glutathione in Alzheimer’s disease[J]J Alzheimer Dis, 2014, 40( 3): 519-529.
doi: 10.3233/jad-132483
[50]   CALHOUNJ D, HUFFMANA M, BELLINSKII, et al.CACNA1H variants are not a cause of monogenic epilepsy[J]Human Mutat, 2020, 41( 6): 1138-1144.
doi: 10.1002/humu.24017
[51]   DANIILG, FERNANDES-ROSAF L, CHEMINJ, et al.CACNA1H mutations are associated with different forms of primary aldosteronism[J]EBioMedicine, 2016, 225-236.
doi: 10.1016/j.ebiom.2016.10.002
[52]   LEMKEJ R, LALD, REINTHALERE M, et al.Mutations in GRIN2A cause idiopathic focal epilepsy with rolandic spikes[J]Nat Genet, 2013, 45( 9): 1067-1072.
doi: 10.1038/ng.2728
[53]   VIEIRAM M, NGUYENT A, WUK, et al.An epilepsy-associated GRIN2A rare variant disrupts CaMKIIα phosphorylation of GluN2A and NMDA receptor trafficking[J]Cell Rep, 2020, 32( 9): 108104.
doi: 10.1016/j.celrep.2020.108104
[54]   JANGY, LEEB, KIMH, et al.Trpm2 ablation accelerates protein aggregation by impaired ADPR and autophagic clearance in the brain[J]Mol Neurobiol, 2019, 56( 5): 3819-3832.
doi: 10.1007/s12035-018-1309-0
[55]   HUH, ZHUT, GONGL, et al.Transient receptor potential melastatin 2 contributes to neuroinflammation and negatively regulates cognitive outcomes in a pilocarpine-induced mouse model of epilepsy[J]Int ImmunoPharmacol, 2020, 106824.
doi: 10.1016/j.intimp.2020.106824
[56]   ZHENGQ, ZHUT, HUH, et al.TRPM2 ion channel is involved in the aggravation of cognitive impairment and down regulation of epilepsy threshold in pentylenetetrazole-induced kindling mice[J]Brain Res Bull, 2020, 48-60.
doi: 10.1016/j.brainresbull.2019.11.018
[57]   VANDE VELDEC, CIZEAUJ, DUBIKD, et al.BNIP3 and genetic control of necrosis-like cell death through the mitochondrial permeability transition pore[J]Mol Cell Biol, 2000, 20( 15): 5454-5468.
doi: 10.1128/mcb.20.15.5454-5468.2000
[58]   SUSINS A, LORENZOH K, ZAMZAMIN, et al.Molecular characterization of mitochondrial apoptosis-inducing factor[J]Nature, 1999, 397( 6718): 441-446.
doi: 10.1038/17135
[59]   ZHUT, ZHAOY, HUH, et al.TRPM2 channel regulates cytokines production in astrocytes and aggravates brain disorder during lipopolysaccharide-induced endotoxin sepsis[J]Int ImmunoPharmacol, 2019, 105836.
doi: 10.1016/j.intimp.2019.105836
[60]   BAILEYJ N, PATTERSONC, DE NIJSL, et al.EFHC1 variants in juvenile myoclonic epilepsy: reanalysis according to NHGRI and ACMG guidelines for assigning disease causality[J]Genet Med, 2017, 19( 2): 144-156.
doi: 10.1038/gim.2016.86
[61]   SUZUKIT, DELGADO-ESCUETAA V, AGUANK, et al.Mutations in EFHC1 cause juvenile myoclonic epilepsy[J]Nat Genet, 2004, 36( 8): 842-849.
doi: 10.1038/ng1393
[62]   LOUCKSC M, PARKK, WALKERD S, et al.EFHC1, implicated in juvenile myoclonic epilepsy, functions at the cilium and synapse to modulate dopamine signaling[J/OL]eLife, 2019, e37271.
doi: 10.7554/eLife.37271
[63]   KATANOM, NUMATAT, AGUANK, et al.The juvenile myoclonic epilepsy-related protein EFHC1 interacts with the redox-sensitive TRPM2 channel linked to cell death[J]Cell Calcium, 2012, 51( 2): 179-185.
doi: 10.1016/j.ceca.2011.12.011
[64]   MAHMUDAN A, YOKOYAMAS, MUNESUET, et al.One single nucleotide polymorphism of the TRPM2 channel gene identified as a risk factor in bipolar disorder associates with autism spectrum disorder in a Japanese population[J]Diseases, 2020, 8( 1): 4.
doi: 10.3390/diseases8010004
[65]   BELROSEJ C, JACKSONM F. TRPM2: a candidate therapeutic target for treating neurological diseases[J]Acta Pharmacol Sin, 2018, 39( 5): 722-732.
doi: 10.1038/aps.2018.31
[66]   HARAGUCHIK, KAWAMOTOA, ISAMIK, et al.TRPM2 contributes to inflammatory and neuropathic pain through the aggravation of pronociceptive inflammatory responses in mice[J]J Neuroscience, 2012, 32( 11): 3931-3941.
doi: 10.1523/JNEUROSCI.4703-11.2012
[67]   HERMOSURAM C, CUIA M, GOR C V, et al.Altered functional properties of a TRPM2 variant in Guamanian ALS and PD[J]Proc Natl Acad Sci U S A, 2008, 105( 46): 18029-18034.
doi: 10.1073/pnas.0808218105
[1] KUANG Wenjing,LUO Xiaobo,WANG Jiongke,ZENG Xin. Research progress on Melkersson-Rosenthal syndrome[J]. J Zhejiang Univ (Med Sci), 2021, 50(2): 148-154.
[2] WANG Chenyu,WANG Yingnan,WANG Cunyi,SHI Jiejun,WANG Huiming. Research progress on tissue engineering in repairing temporo-mandibular joint[J]. J Zhejiang Univ (Med Sci), 2021, 50(2): 212-221.
[3] REN Chaojie,ZHONG Danni,ZHOU Min. Research progress on the biomedical application of microalgae[J]. J Zhejiang Univ (Med Sci), 2021, 50(2): 261-266.
[4] SHAO Yiming,SU Lide,HAO Rui,WANG Qianqian,NARANMANDURA Hua. Advances on molecular mechanism of hepatitis B virus-induced hepatocellular carcinoma[J]. J Zhejiang Univ (Med Sci), 2021, 50(1): 113-122.
[5] HAN Hengyi,FENG Fan,LI Haitao. Research advances on epigenetics and cancer metabolism[J]. J Zhejiang Univ (Med Sci), 2021, 50(1): 1-16.
[6] CHEN Fei,YU Min,ZHONG Yonghong,HUA Wen,HUANG Huaqiong. The role of neutrophils in asthma[J]. J Zhejiang Univ (Med Sci), 2021, 50(1): 123-130.
[7] YAN Jing,ZHANG Tingting,ZHAO Kui. Application of molecular probes in nuclear imaging of neuroendocrine tumors[J]. J Zhejiang Univ (Med Sci), 2021, 50(1): 131-137.
[8] ZHANG Mingquan,PAN Junchen,HUANG Peng. Interaction between RAS gene and lipid metabolism in cancer[J]. J Zhejiang Univ (Med Sci), 2021, 50(1): 17-22.
[9] HU Xinyang,JIN Hongchuan,ZHU Liyuan. Effect of glutamine metabolism on chemoresistance and its mechanism in tumors[J]. J Zhejiang Univ (Med Sci), 2021, 50(1): 32-40.
[10] MENG Ying,WANG Qifei,LYU Zhimin. Cholesterol metabolism and tumor[J]. J Zhejiang Univ (Med Sci), 2021, 50(1): 23-31.
[11] ZHU Huiqi,YING Kejing. Tissue factors and venous thromboembolism in cancer patients[J]. J Zhejiang Univ (Med Sci), 2020, 49(6): 772-778.
[12] LIN Cuicui,CHEN Zhengyun,WANG Chunyan,XI Yongmei. Research progress on biomarkers for endometriosis based on lipidomics[J]. J Zhejiang Univ (Med Sci), 2020, 49(6): 779-784.
[13] LI Mengyao,LIU Pan,KE Yuehai,ZHANG Xue. Research progress on macrophage in radiation induced lung injury[J]. J Zhejiang Univ (Med Sci), 2020, 49(5): 623-628.
[14] HAN Xue,JIANG Guojun,SHI Qiaojuan. Effects of antihyperglycemics on endothelial progenitor cells[J]. J Zhejiang Univ (Med Sci), 2020, 49(5): 629-636.
[15] DUAN Runping,XU Yesheng,ZHENG Libin,YAO Yufeng. Research progress on etiologic diagnosis of ocular viral diseases[J]. J Zhejiang Univ (Med Sci), 2020, 49(5): 644-650.