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Gasdermin Family: a Promising Therapeutic Target for Stroke

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Abstract

Stroke is one of the leading causes of death worldwide and therapies are limited. According to the mechanisms underlying stroke, direct cell demise, destruction of organelles, blood-brain barrier disruption, neuroinflammation are potential therapeutic targets. Gasdermin (GSDM) family is a series of recently discovered proteins, which acts as the executor of pyroptosis and protagonist of membrane pore formation. It can be cleaved by inflammatory caspases that are activated by multi-protein complexes, named as inflammasomes, and divided into two domains. The N-terminal domain interacts with lipid localized in the plasma membrane as well as organelle membrane and perforates them. After the formation of pores, the dysfunctional structures suffer lytic death and their contents are released. In this review, we discuss the biological characteristic of GSDM family and their possible roles in stroke-induced brain injury, and based on the review, we hypothesize the feasibility of using GSDMs as a potential target for stroke treatment.

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References

  1. Roy-O'Reilly M, Ritzel RM, Conway SE, Staff I, et al. CCL11 (Eotaxin-1) levels predict long-term functional outcomes in patients following ischemic stroke. Transl Stroke Res. 2017;8(6):578–84.

    Article  CAS  Google Scholar 

  2. Damani RH, Anand S, Asgarisabet P, Bissell C, Savitz S, Suarez JI. Regional intervention of stroke care to increase thrombolytic therapy for acute ischemic stroke: the Southeast Texas experience. Stroke. 2018;49:2008–10. https://doi.org/10.1161/STROKEAHA.118.021109.

    Article  PubMed  Google Scholar 

  3. Benjamin EJ, Virani SS, Callaway CW, et al. Heart disease and stroke statistics—2018 update: a report from the American Heart Association. Circulation. 2018;137(12):e67–492.

    Article  Google Scholar 

  4. She DT, Jo DG, Arumugam TV. Emerging roles of Sirtuins in ischemic stroke. Transl Stroke Res. 2017;8:405–23. https://doi.org/10.1007/s12975-017-0544-4.

    Article  CAS  Google Scholar 

  5. Alhadidi Q, Bin Sayeed MS, Shah ZA. Cofilin as a promising therapeutic target for ischemic and hemorrhagic stroke. Transl Stroke Res. 2016;7:33–41.

    Article  CAS  Google Scholar 

  6. Moskowitz MA, Lo EH, Iadecola C. The science of stroke: mechanisms in search of treatments. Neuron. 2010;67(2):181–98.

    Article  CAS  Google Scholar 

  7. George PM, Steinberg GK. Novel stroke therapeutics: unraveling stroke pathophysiology and its impact on clinical treatments. Neuron. 2015;87(2):297–309.

    Article  CAS  Google Scholar 

  8. Magistretti PJ, Allaman I. A cellular perspective on brain energy metabolism and functional imaging. Neuron. 2015;86(4):883–901.

    Article  CAS  Google Scholar 

  9. Song M, Yu SP. Ionic regulation of cell volume changes and cell death after ischemic stroke. Transl Stroke Res. 2014;5(1):17–27.

    Article  CAS  Google Scholar 

  10. Dirnagl U, Iadecola C, Moskowitz MA. Pathobiology of ischaemic stroke: an integrated view. Trends Neurosci. 1999;22(9):391–7.

    Article  CAS  Google Scholar 

  11. Kalogeris T, Bao Y, Korthuis RJ. Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning. Redox Biol. 2014;2:702–14.

    Article  CAS  Google Scholar 

  12. Klimova N, Long A, Kristian T. Significance of mitochondrial protein post-translational modifications in pathophysiology of brain injury. Transl Stroke Res. 2018;9(3):223–37.

    Article  Google Scholar 

  13. Shichita T, Ito M, Yoshimura A. Post-ischemic inflammation regulates neural damage and protection. Front Cell Neurosci. 2014;8:319.

    Article  Google Scholar 

  14. Seifert HA, Pennypacker KR. Molecular and cellular immune responses to ischemic brain injury. Transl Stroke Res. 2014;5(5):543–53.

    Article  CAS  Google Scholar 

  15. Atangana E, Schneider UC, Blecharz K, Magrini S, Wagner J, Nieminen-Kelhä M, et al. Intravascular inflammation triggers intracerebral activated microglia and contributes to secondary brain injury after experimental subarachnoid hemorrhage (eSAH). Transl Stroke Res. 2017;8(2):144–56.

    Article  CAS  Google Scholar 

  16. Shi YJ, Leak RK, Keep RF, Chen J. Translational stroke research on blood-brain barrier damage: challenges, perspectives, and goals. Transl Stroke Res. 2016;7:89–92.

    Article  Google Scholar 

  17. Lo EH, Dalkara T, Moskowitz MA. Mechanisms, challenges and opportunities in stroke. Nat Rev Neurosci. 2003;4(5):399–415.

    Article  CAS  Google Scholar 

  18. Boltze J, Ayata C. Challenges and controversies in translational stroke research - an introduction. Transl Stroke Res. 2016;7(5):355–7.

    Article  Google Scholar 

  19. Bergsbaken T, Fink SL, Cookson BT. Pyroptosis: host cell death and inflammation. Nat Rev Microbiol. 2009;7(2):99–109.

    Article  CAS  Google Scholar 

  20. Wallach D, Kang TB, Dillon CP, Green DR. Programmed necrosis in inflammation: toward identification of the effector molecules. Science. 2016;352:aaf2154. https://doi.org/10.1126/science.aaf2154.

    Article  CAS  PubMed  Google Scholar 

  21. Zhang Y, Chen X, Gueydan C, Han J. Plasma membrane changes during programmed cell deaths. Cell Res. 2018;28(1):9–21.

    Article  CAS  Google Scholar 

  22. Chen X, He WT, Hu LC, Li J, Fang Y, Wang X, et al. Pyroptosis is driven by non-selective gasdermin-D pore and its morphology is different from MLKL channel-mediated necroptosis. Cell Res. 2016;26:1007–20.

    Article  CAS  Google Scholar 

  23. Russo HM, Rathkey J, Boyd-Tressler A, Katsnelson MA, Abbott DW, Dubyak GR. Active caspase-1 induces plasma membrane pores that precede pyroptotic lysis and are blocked by lanthanides. J Immunol. 2016;197(4):1353–67.

    Article  CAS  Google Scholar 

  24. Evavold CL, Ruan J, Tan Y, Xia S, et al. The pore-forming protein gasdermin d regulates interleukin-1 secretion from living macrophages. Immunity. 2018;48(1):35–44.e6.

    Article  CAS  Google Scholar 

  25. Shi J, Gao W, Shao F. Pyroptosis: gasdermin-mediated programmed necrotic cell death. Trends Biochem Sci. 2017;42(4):245–54.

    Article  CAS  Google Scholar 

  26. Kayagaki N, Stowe IB, Lee BL, O’Rourke K, Anderson K, Warming S, et al. Caspase-11 cleaves gasdermin D for non-canonical inflammasome signaling. Nature. 2015;526:666–71.

    Article  CAS  Google Scholar 

  27. Shi J, Zhao Y, Wang K, Shi X, Wang Y, Huang H, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature. 2015;526(7575):660–5.

    Article  CAS  Google Scholar 

  28. Liu X, Zhang Z, Ruan J, Pan Y, Magupalli VG, Wu H, et al. Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores. Nature. 2016;535(7610):153–8.

    Article  CAS  Google Scholar 

  29. Aglietti RA, Estevez A, Gupta A, Ramirez MG, Liu PS, Kayagaki N, et al. GsdmD p30 elicited by caspase-11 during pyroptosis forms pores in membranes. Proc Natl Acad Sci U S A. 2016;113(28):7858–63.

    Article  CAS  Google Scholar 

  30. Sborgi L, Rühl S, Mulvihill E, Pipercevic J, Heilig R, Stahlberg H, et al. GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death. EMBO J. 2016;35(16):1766–78.

    Article  CAS  Google Scholar 

  31. Ding J, Wang K, Liu W, She Y, Sun Q, Shi J, et al. Pore-forming activity and structural autoinhibition of the gasdermin family. Nature. 2016;535(7610):111–6.

    Article  CAS  Google Scholar 

  32. Walsh JG, Muruve DA, Power C. Inflammasomes in the CNS. Nat Rev Neurosci. 2014;15:84–9.

    Article  CAS  Google Scholar 

  33. Barrington J, Lemarchand E, Allan SM. A brain in flame; do inflammasomes and pyroptosis influence stroke pathology? Brain Pathol. 2017;27(2):205–12.

    Article  Google Scholar 

  34. Kuang S, Zheng J, Yang H, Li S, Duan S, Shen Y, et al. Structure insight of GSDMD reveals the basis of GSDMD autoinhibition in cell pyroptosis. Proc Natl Acad Sci U S A. 2017;114(40):10642–7.

    Article  CAS  Google Scholar 

  35. Ruan J, Xia S, Liu X, Lieberman J, Wu H. Cryo-EM structure of the gasdermin A3 membrane pore. Nature. 2018;557(7703):62–7.

    Article  CAS  Google Scholar 

  36. Delmaghani S, del Castillo EJ, Michel V, Leibovici M, et al. Mutations in the gene encoding pejvakin, a newly identified protein of the afferent auditory pathway, cause DFNB59 auditory neuropathy. Nat Genet. 2006;38(7):770–8.

    Article  CAS  Google Scholar 

  37. Saeki N, Sasaki H. Gasdermin superfamily: a novel gene family functioning in epithelial cells. In: Carrasco J, Matheus M, editors. Endothelium and Epithelium: Composition, Functions, and Pathology. New York: Nova Science Publishers; 2011. pp. 193–211.

  38. Lee SW, Gajavelli S, Spurlock MS, Andreoni C, de Rivero Vaccari JP, Bullock MR, et al. Microglial inflammasome activation in penetrating ballistic-like brain injury. J Neurotrauma. 2018;35(14):1681–93.

    Article  Google Scholar 

  39. Ge X, Li W, Huang S, Yin Z, Xu X, Chen F, et al. The pathological role of NLRs and AIM2 inflammasome-mediated pyroptosis in damaged blood-brain barrier after traumatic brain injury. Brain Res. 2018;1697:10–20. https://doi.org/10.1016/j.brainres.2018.06.008.

    Article  CAS  PubMed  Google Scholar 

  40. McKenzie BA, Mamik MK, Saito LB, Boghozian R, et al. Caspase-1 inhibition prevents glial inflammasome activation and pyroptosis in models of multiple sclerosis. Proc Natl Acad Sci U S A. 2018;115:E6065–74. https://doi.org/10.1073/pnas.1722041115.

    Article  CAS  PubMed  Google Scholar 

  41. Martinon F, Burns K, Tschopp J. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-β. Mol Cell. 2002;10(2):417–26.

    Article  CAS  Google Scholar 

  42. Rathinam VA, Vanaja SK, Fitzgerald KA. Regulation of inflammasome signaling. Nat Immunol. 2012;13(4):333–42.

    Article  CAS  Google Scholar 

  43. Srinivasula SM, Poyet JL, Razmara M, Datta P, Zhang ZJ, Alnemri ES. The PYRIN-CARD protein ASC is an activating adaptor for caspase-1. J Biol Chem. 2002;277:21119–22.

    Article  CAS  Google Scholar 

  44. Stehlik C, Lee SH, Dorfleutner A, Stassinopoulos A, Sagara J, Reed JC. Apoptosis-associated speck-like protein containing a caspase recruitment domain is a regulator of procaspase-1 activation. J Immunol. 2003;171:6154–63.

    Article  CAS  Google Scholar 

  45. Mariathasan S, Newton K, Monack DM, Vucic D, French DM, Lee WP, et al. Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf. Nature. 2004;430:213–8.

    Article  CAS  Google Scholar 

  46. Kayagaki N, Wong MT, Stowe IB, Ramani SR, Gonzalez LC, Akashi-Takamura S, et al. Noncanonical inflammasome activation by intracellular LPS independent of TLR4. Science. 2013;341:1246–9.

    Article  CAS  Google Scholar 

  47. Kayagaki N, Warming S, Lamkanfi M, Walle LV, Louie S, Dong J, et al. Non-canonical inflammasome activation targets caspase-11. Nature. 2011;479:117–21.

    Article  CAS  Google Scholar 

  48. Petrilli V, et al. Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration. Cell Death Differ. 2007;14:1583–9.

    Article  CAS  Google Scholar 

  49. Rühl S, Broz P. Caspase-11 activates a canonical NLRP3 inflammasome by promoting K+ efflux. Eur J Immunol. 2015;45:2927–36.

    Article  Google Scholar 

  50. Chen S, Yang Q, Chen G, Zhang JH. An update on inflammation in the acute phase of intracerebral hemorrhage. Transl Stroke Res. 2015;6(1):4–8.

    Article  CAS  Google Scholar 

  51. Abulafia DP, de Rivero Vaccari JP, Lozano JD, Lotocki G, Keane RW, Dietrich WD. Inhibition of the inflammasome complex reduces the inflammatory response after thromboembolic stroke in mice. J Cereb Blood Flow Metab. 2009;29(3):534–44.

    Article  CAS  Google Scholar 

  52. Mortezaee K, Khanlarkhani N, Beyer C, Zendedel A. Inflammasome: its role in traumatic brain and spinal cord injury. J Cell Physiol. 2018;233(7):5160–9.

    Article  CAS  Google Scholar 

  53. Denes A, Coutts G, Lénárt N, Cruickshank SM, Pelegrin P, Skinner J, et al. AIM2 and NLRC4 inflammasomes contribute with ASC to acute brain injury independently of NLRP3. Proc Natl Acad Sci U S A. 2015;112(13):4050–5.

    Article  CAS  Google Scholar 

  54. Ma Q, Chen S, Hu Q, Feng H, Zhang JH, Tang J. NLRP3 inflammasome contributes to inflammation after intracerebral hemorrhage. Ann Neurol. 2014;75(2):209–19.

    Article  CAS  Google Scholar 

  55. Chen S, Ma Q, Krafft PR, Hu Q, Rolland W II, Sherchan P, et al. P2X7R/cryopyrin inflammasome axis inhibition reduces neuroinflammation after SAH. Neurobiol Dis. 2013;58:296–307.

    Article  CAS  Google Scholar 

  56. Friedlander RM, Gagliardini V, Hara H, Fink KB, Li W, MacDonald G, et al. Expression of a dominant negative mutant of interleukin-1 beta converting enzyme in transgenic mice prevents neuronal cell death induced by trophic factor withdrawal and ischemic brain injury. J Exp Med. 1997;185(5):933–40.

    Article  CAS  Google Scholar 

  57. Schielke GP, Yang GY, Shivers BD, Betz AL. Reduced ischemic brain injury in interleukin-1 beta converting enzyme-deficient mice. J Cereb Blood Flow Metab. 1998;18:180–5.

    Article  CAS  Google Scholar 

  58. de Rivero Vaccari JP, Lotocki G, Marcillo AE, Dietrich WD, Keane RW. A molecular platform in neurons regulates inflammation after spinal cord injury. J Neurosci. 2008;28:3404–14.

    Article  Google Scholar 

  59. Kang SJ, Wang S, Hara H, Peterson EP, Namura S, Amin-Hanjani S, et al. Dual role of caspase-11 in mediating activation of caspase-1 and caspase-3 under pathological conditions. J Cell Biol. 2000;149(3):613–22.

    Article  CAS  Google Scholar 

  60. Kovacs SB, Miao EA. Gasdermins: effectors of pyroptosis. Trends Cell Biol. 2017;27(9):673–84.

    Article  CAS  Google Scholar 

  61. Wei H, Li Y, Han S, Liu S, et al. cPKCγ-modulated autophagy in neurons alleviates ischemic injury in brain of mice with ischemic stroke through Akt-mTOR pathway. Transl Stroke Res. 2016;7(6):497–511.

    Article  CAS  Google Scholar 

  62. Shi L, Al-Baadani A, Zhou K, Shao A, et al. PCMT1 ameliorates neuronal apoptosis by inhibiting the activation of MST1 after subarachnoid hemorrhage in rats. Transl Stroke Res. 2017;8:474–83. https://doi.org/10.1007/s12975-017-0540-8.

    Article  CAS  Google Scholar 

  63. Chao KL, Kulakova L, Herzberg O. Gene polymorphism linked to increased asthma and IBD risk alters gasdermin-B structure, a sulfatide and phosphoinositide binding protein. Proc Natl Acad Sci U S A. 2017;114(7):E1128–37.

    Article  CAS  Google Scholar 

  64. Wang Y, Gao W, Shi X, Ding J, Liu W, He H, et al. Chemotherapy drugs induce pyroptosis through caspase-3 cleavage of a gasdermin. Nature. 2017;547(7661):99–103.

    Article  CAS  Google Scholar 

  65. Van Laer L, Huizing EH, Verstreken M, van Zuijlen D, et al. Nonsyndromic hearing impairment is associated with a mutation in DFNA5. Nat Genet. 1998;20(2):194–7.

    Article  Google Scholar 

  66. Van Laer L, Pfister M, Thys S, Vrijens K, et al. Mice lacking Dfna5 show a diverging number of cochlear fourth row outer hair cells. Neurobiol Dis. 2005;19(3):386–99.

    Article  Google Scholar 

  67. Cheng KT, Xiong S, Ye Z, Hong Z, di A, Tsang KM, et al. Caspase-11-mediated endothelial pyroptosis underlies endotoxemia-induced lung injury. J Clin Invest. 2017;127(11):4124–35.

    Article  Google Scholar 

  68. Abbott NJ, Patabendige AA, Dolman DE, Yusof SR, Begley DJ. Structure and function of the blood–brain barrier. Neurobiol Dis. 2010;37(1):13–25.

    Article  CAS  Google Scholar 

  69. Shi Y, Zhang L, Pu H, Mao L, Hu X, Jiang X, et al. Rapid endothelial cytoskeletal reorganization enables early blood–brain barrier disruption and long-term ischaemic reperfusion brain injury. Nat Commun. 2016;7:10523.

    Article  CAS  Google Scholar 

  70. Sobowale OA, Parry-Jones AR, Smith CJ, Tyrrell PJ, et al. Interleukin-1 in stroke from bench to bedside. Stroke. 2016;47:2160–7.

    Article  Google Scholar 

  71. McCann SK, Cramond F, Macleod MR, Sena ES. Systematic review and meta-analysis of the efficacy of interleukin-1 receptor antagonist in animal models of stroke: an update. Transl Stroke Res. 2016;7(5):395–406.

    Article  CAS  Google Scholar 

  72. Fu Y, Liu Q, Anrather J, Shi FD. Immune interventions in stroke. Nat Rev Neurol. 2015;11(9):524–35.

    Article  CAS  Google Scholar 

  73. Palladino MA, Bahjat FR, Theodorakis EA, Moldawer LL. Anti-TNF-α therapies: the next generation. Nat Rev Drug Discov. 2003;2(9):736–46.

    Article  CAS  Google Scholar 

  74. Simpson RJ, Hammacher A, Smith DK, Matthews JM, Ward LD. Interleukin-6: structure-function relationships. Protein Sci. 1997;6(5):929–55.

    Article  CAS  Google Scholar 

  75. Lambertsen KL, Biber K, Finsen B. Inflammatory cytokines in experimental and human stroke. J Cereb Blood Flow Metab. 2012;32(9):1677–98.

    Article  CAS  Google Scholar 

  76. van Meer G, Voelker DR, Feigenson GW. Membrane lipids: where they are and how they behave. Nat Rev Mol Cell Biol. 2008;9(2):112–24.

    Article  Google Scholar 

  77. Vosler PS, Graham SH, Wechsler LR, Chen J. Mitochondrial targets for stroke focusing basic science research toward development of clinically translatable therapeutics. Stroke. 2009;40(9):3149–55.

    Article  CAS  Google Scholar 

  78. Bergsbaken T, Fink SL, den Hartigh AB, Loomis WP, Cookson BT. Coordinated host responses during pyroptosis: caspase-1-dependent lysosome exocytosis and inflammatory cytokine maturation. J Immunol. 2011;187(5):2748–54.

    Article  CAS  Google Scholar 

  79. von Moltke J, Trinidad NJ, Moayeri M, Kintzer AF, Wang SB, van Rooijen N, et al. Rapid induction of inflammatory lipid mediators by the inflammasome in vivo. Nature. 2012;490(7418):107–11.

    Article  Google Scholar 

  80. Bell JD, Cho JE, Giffard RG. MicroRNA changes in preconditioning-induced neuroprotection. Transl Stroke Res. 2017;8(6):585–96.

    Article  CAS  Google Scholar 

  81. Xin Q, Ji B, Cheng B, Wang C, Liu H, Chen X, et al. Endoplasmic reticulum stress in cerebral ischemia. Neurochem Int. 2014;68:18–27.

    Article  CAS  Google Scholar 

  82. Jiang Z, Hu Z, Zeng L, Lu W, et al. The role of the Golgi apparatus in oxidative stress: is this organelle less significant than mitochondria? Free Radic Biol Med. 2011;50(8):907–17.

    Article  CAS  Google Scholar 

  83. Sun N, Keep RF, Hua Y, Xi G. Critical role of the sphingolipid pathway in stroke: a review of current utility and potential therapeutic targets. Transl Stroke Res. 2016;7(5):420–38.

    Article  CAS  Google Scholar 

  84. Egawa N, Lok J, Washida K, Arai K. Mechanisms of axonal damage and repair after central nervous system injury. Transl Stroke Res. 2017;8(1):14–21.

    Article  CAS  Google Scholar 

  85. Delmaghani S, Defourny J, Aghaie A, Beurg M, Dulon D, Thelen N, et al. Hypervulnerability to sound exposure through impaired adaptive proliferation of peroxisomes. Cell. 2015;163(4):894–906.

    Article  CAS  Google Scholar 

  86. Rogers C, Fernandes-Alnemri T, Mayes L, Alnemri D, Cingolani G, Alnemri ES. Cleavage of DFNA5 by caspase-3 during apoptosis mediates progression to secondary necrotic/pyroptotic cell death. Nat Commun. 2017;8:14128.

    Article  CAS  Google Scholar 

  87. Wu C, Orozco C, Boyer J, Leglise M, Goodale J, Batalov S, et al. BioGPS: an extensible and customizable portal for querying and organizing gene annotation resources. Genome Biol. 2009;10:R130.

    Article  Google Scholar 

  88. Nikoletopoulou V, Markaki M, Palikaras K, Tavernarakis N. Crosstalk between apoptosis, necrosis and autophagy. Biochim Biophys Acta. 2013;1833(12):3448–59.

    Article  CAS  Google Scholar 

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Funding

This study was funded by the National Natural Science Foundation of China (81500992), Natural Science Foundation of Zhejiang (LQ16H090002), Medical and Health Key Project of Zhejiang Province (2016RCA015).

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Authors and Affiliations

  1. Department of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, NO.88 Jiefang Rd, Hangzhou, 310009, China

    Sheng Chen, Shuhao Mei, Yujie Luo, Jianmin Zhang & Junming Zhu

  2. Department of Neurosurgery, Taizhou Hospital, Wenzhou Medical University, Linhai, Zhejiang, China

    Sheng Chen

  3. Department of Neurosurgery, Stanford University, Stanford, CA, USA

    Hemmings Wu

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  1. Sheng Chen
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Contributions

Sheng Chen and Dr. Shuhao Mei contributed equally to the study. JunMing Zhu was the principal investigator. Sheng Chen and Shuhao Mei wrote the paper and made the original figures. Yujie Luo, Hemmings Wu, and Jianmin Zhang critically revised the texts and figures.

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Correspondence to Junming Zhu.

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Chen, S., Mei, S., Luo, Y. et al. Gasdermin Family: a Promising Therapeutic Target for Stroke. Transl. Stroke Res. 9, 555–563 (2018). https://doi.org/10.1007/s12975-018-0666-3

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