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    {
      "pmid": "35642214",
      "doi": "10.2147/JIR.S350109",
      "abstract": "1. J Inflamm Res. 2022 May 25;15:3083-3094. doi: 10.2147/JIR.S350109. eCollection\n 2022.\n\nMicroglia-Mediated Neuroinflammation: A Potential Target for the Treatment of \nCardiovascular Diseases.\n\nWang M(#)(1)(2)(3), Pan W(#)(1)(2)(3), Xu Y(#)(1)(2)(3), Zhang J(1)(2)(3), Wan \nJ(1)(2)(3), Jiang H(1)(2)(3).\n\nAuthor information:\n(1)Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, \nPeople's Republic of China.\n(2)Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, People's \nRepublic of China.\n(3)Hubei Key Laboratory of Cardiology, Wuhan, 430060, People's Republic of \nChina.\n(#)Contributed equally\n\nMicroglia are tissue-resident macrophages of the central nervous system (CNS). \nIn the CNS, microglia play an important role in the monitoring and intervention \nof synaptic and neuron-level activities. Interventions targeting microglia have \nbeen shown to improve the prognosis of various neurological diseases. Recently, \nstudies have observed the activation of microglia in different cardiovascular \ndiseases. In addition, different approaches that regulate the activity of \nmicroglia have been shown to modulate the incidence and progression of \ncardiovascular diseases. The change in autonomic nervous system activity after \nneuroinflammation may be a potential intermediate link between microglia and \ncardiovascular diseases. Here, in this review, we will discuss recent updates on \nthe regulatory role of microglia in hypertension, myocardial infarction and \nischemia/reperfusion injury. We propose that microglia serve as neuroimmune \nmodulators and potential targets for cardiovascular diseases.\n\n© 2022 Wang et al.\n\nDOI: 10.2147/JIR.S350109\nPMCID: PMC9148574\nPMID: 35642214\n\nConflict of interest statement: The authors declare that they have no competing \ninterests. References1.KapoorK, BhandareAM, FarnhamMMJ, et al. Alerted microglia \nand the sympathetic nervous system: a novel form of microglia in the development \nof hypertension. Respir Physiol Neurobiol. 2016;226:51–62. \ndoi:10.1016/j.resp.2015.11.015266440792.BadoerE. Microglia: activation in acute \nand chronic inflammatory states and in response to cardiovascular dysfunction. \nInt J Biochem Cell Biol. 2010;42(10):1580–1585. \ndoi:10.1016/j.biocel.2010.07.005206384853.SavchenkoVL, McKannaJA, NikonenkoIR, \net al. Microglia and astrocytes in the adult rat brain: comparative \nimmunocytochemical analysis demonstrates the efficacy of lipocortin 1 \nimmunoreactivity. Neuroscience. 2000;96(1):195–203. \ndoi:10.1016/S0306-4522(99)00538-2106834234.WolfSA, BoddekeHWGM, KettenmannH. \nMicroglia in physiology and disease. Annu Rev Physiol. 2017;79(1):619–643. \ndoi:10.1146/annurev-physiol-022516-034406279596205.LevickSP, MurrayDB, \nJanickiJS, et al. Sympathetic nervous system modulation of inflammation and \nremodeling in the hypertensive heart. Hypertension. 2010;55(2):270–276. \ndoi:10.1161/HYPERTENSIONAHA.109.142042200481966.DengY, TanX, LiML, et al. \nAngiotensin-converting enzyme 2 in the rostral ventrolateral medulla regulates \ncholinergic signaling and cardiovascular and sympathetic responses in \nhypertensive rats. Neurosci Bull. 2019;35(1):67–78. \ndoi:10.1007/s12264-018-0298-3303185627.YoungCN, DavissonRL. Angiotensin-II, the \nbrain, and hypertension: an update. Hypertension. 2015;66(5):920–926. \ndoi:10.1161/HYPERTENSIONAHA.115.03624263245088.WangM, LiS, ZhouX, et al. \nIncreased inflammation promotes ventricular arrhythmia through aggravating left \nstellate ganglion remodeling in a canine ischemia model. Int J Cardiol. \n2017;248:286–293. doi:10.1016/j.ijcard.2017.08.011288268009.WangY, JiangW, \nChenH, et al. Sympathetic nervous system mediates cardiac remodeling after \nmyocardial infarction in a circadian disruption model. Front Cardiovasc Med. \n2021;8:668387. doi:10.3389/fcvm.2021.6683873384256610.CooteJH, ChauhanRA. The \nsympathetic innervation of the heart: important new insights. Auton Neurosci. \n2016;199:17–23. doi:10.1016/j.autneu.2016.08.0142756899511.CronkJC, KipnisJ. \nMicroglia – the brain’s busy bees. F1000Prime Rep. 2013;5. \ndoi:10.12703/P5-5312.AjamiB, BennettJL, KriegerC, et al. Local self-renewal can \nsustain CNS microglia maintenance and function throughout adult life. Nat \nNeurosci. 2007;10(12):1538–1543. doi:10.1038/nn20141802609713.DubbelaarML, \nKrachtL, EggenBJL, et al. The kaleidoscope of microglial phenotypes. Front \nImmunol. 2018;9:1753. doi:10.3389/fimmu.2018.017533010858614.NimmerjahnA, \nKirchhoffF, HelmchenF. Resting microglial cells are highly dynamic surveillants \nof brain parenchyma in vivo. Science. 2005;308(5726):1314–1318. \ndoi:10.1126/science.11106471583171715.von BernhardiR, HerediaF, SalgadoN, et al. \nMicroglia function in the normal brain. Adv Exp Med Biol. \n2016;949:67.2771468516.CherryJD, OlschowkaJA, BanionMO. Neuroinflammation and M2 \nmicroglia: the good, the bad, and the inflamed. J Neuroinflammation. \n2014;11(1):98. doi:10.1186/1742-2094-11-982488988617.Marin-TevaJL, DusartI, \nColinC, et al. Microglia",
      "journal": "J Inflamm Res",
      "year": 2022,
      "authors": "Wang M, Pan W, Xu Y, Zhang J, Wan J, Jiang H",
      "url": "https://pubmed.ncbi.nlm.nih.gov/35642214",
      "external_ids": {
        "doi": "10.2147/JIR.S350109",
        "pmid": "35642214"
      },
      "citation_count": 1,
      "domain": "neurodegeneration"
    }