Ischemic stroke is a common neurological disease with the characteristics of high morbidity, high mortality and high recurrence, and its pathogenesis has been one of the hot spots of research. In recent years, with the continuous development of neuroscience and biomedical research methods, a lot of progress has been made in the study of the pathogenesis of ischemic stroke. This paper reviews the literature on the pathogenesis of ischemic stroke at home and abroad in recent years, and summarizes the pathophysiological changes involved in the development of ischemic stroke and the risk factors that may lead to its occurrence and progression, to better understand the pathogenesis of ischemic stroke and provide more effective means for its prevention and treatment.

Yang Ruting, Bi Sheng. Advances in the study of the pathogenesis of ischemic stroke. International Journal of Frontiers in Medicine (2023), Vol. 5, Issue 4: 81-85. https://doi.org/10.25236/IJFM.2023.050413.

[1] Wu Jiang. Neurology [M]. People's Health Publishing House, 2005

[2] Saini V, Guada L, Yavagal D R. Global Epidemiology of Stroke and Access to Acute Ischemic Stroke Interventions[J]. Neurology, 2021, 97(20 Suppl 2): S6–S16.

[3] Hankey G J. Stroke[J]. Lancet (London, England), 2017, 389(10069): 641–654.

[4] Meschia J F, Bushnell C, Boden-Albala B, et al. Guidelines for the primary prevention of stroke: a statement for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2014, 45(12): 3754–3832.

[5] Isabel C, Calvet D, Mas J-L. Stroke prevention[J]. Presse Medicale (Paris, France: 1983), 2016, 45(12 Pt 2): e457–e471.

[6] Arteaga C L, Sliwkowski M X, Osborne C K, et al. Treatment of HER2-positive breast cancer: current status and future perspectives[J]. Nature Reviews. Clinical Oncology, 2011, 9(1): 16–32.

[7] Regenhardt R W, Das A S, Lo E H, et al. Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review[J]. JAMA neurology, 2018, 75(10): 1273–1281.

[8] Yamada Y, Fuku N, Tanaka M, et al. Identification of CELSR1 as a susceptibility gene for ischemic stroke in Japanese individuals by a genome-wide association study[J]. Atherosclerosis, 2009, 207(1): 144–149.

[9] Kubo M, Hata J, Ninomiya T, et al. A nonsynonymous SNP in PRKCH (protein kinase C eta) increases the risk of cerebral infarction[J]. Nature Genetics, 2007, 39(2): 212–217.

[10] Lee T-H, Ko T-M, Chen C-H, et al. Identification of PTCSC3 as a Novel Locus for Large-Vessel Ischemic Stroke: A Genome-Wide Association Study[J]. Journal of the American Heart Association, 2016, 5(3): e003003.

[11] Sun L, Zhang Z, Ma M, et al. A quantitative assessment of the association between 1425G/A polymorphism in PRKCH and risk of stroke[J]. Neuromolecular Medicine, 2014, 16(4): 814–820.

[12] NINDS Stroke Genetics Network (SiGN), International Stroke Genetics Consortium (ISGC). Loci associated with ischaemic stroke and its subtypes (SiGN): a genome-wide association study[J]. The Lancet. Neurology, 2016, 15(2): 174–184.

[13] Steffensen L B, Rasmussen L M. A role for collagen type IV in cardiovascular disease?[J]. American Journal of Physiology. Heart and Circulatory Physiology, 2018, 315(3): H610–H625.

[14] Cui Y, Zhang Y, Zhao X, et al. ACSL4 exacerbates ischemic stroke by promoting ferroptosis-induced brain injury and neuroinflammation[J]. Brain, Behavior, and Immunity, 2021, 93: 312–321.

[15] Delgado-Rizo V, Martínez-Guzmán M A, Iñiguez-Gutierrez L, et al. Neutrophil Extracellular Traps and Its Implications in Inflammation: An Overview[J]. Frontiers in Immunology, 2017, 8: 81.

[16] Ao L-Y, Yan Y-Y, Zhou L, et al. Immune Cells After Ischemic Stroke Onset: Roles, Migration, and Target Intervention[J]. Journal of molecular neuroscience: MN, 2018, 66(3): 342–355.

[17] Lakhan S E, Kirchgessner A, Tepper D, et al. Matrix metalloproteinases and blood-brain barrier disruption in acute ischemic stroke[J]. Frontiers in Neurology, 2013, 4: 32.

[18] Pennypacker K R. Targeting the peripheral inflammatory response to stroke: role of the spleen[J]. Translational Stroke Research, 2014, 5(6): 635–637.

[19] Men X, Li J, Zhang B, et al. Homocysteine and C-reactive protein associated with progression and prognosis of intracranial branch atheromatous disease[J]. PloS One, 2013, 8(9): e73030.

[20] Moretti R, Caruso P. The Controversial Role of Homocysteine in Neurology: From Labs to Clinical Practice[J]. International Journal of Molecular Sciences, 2019, 20(1): E231.

[21] Gungor L, Polat M, Ozberk M B, et al. Which Ischemic Stroke Subtype Is Associated with Hyperhomocysteinemia?[J]. Journal of Stroke and Cerebrovascular Diseases: The Official Journal of National Stroke Association, 2018, 27(7): 1921–1929.

[22] Chen S, Dong Z, Cheng M, et al. Homocysteine exaggerates microglia activation and neuroinflammation through microglia localized STAT3 overactivation following ischemic stroke[J]. Journal of Neuroinflammation, 2017, 14(1): 187.

[23] Zhang Ailing, Feng Laihui, Teng Junfang, etc Study on polymorphism of methionine synthase reductase gene in middle-aged and young patients with cerebral infarction [J]. Chinese Journal of Neuromedicine, 2012 (01): 37 – 41.

[24] Seo W-K, Seok H-Y, Kim J H, et al. C-reactive protein is a predictor of early neurologic deterioration in acute ischemic stroke[J]. Journal of Stroke and Cerebrovascular Diseases: The Official Journal of National Stroke Association, 2012, 21(3): 181–186.

[25] Cai Z, He W, Zhuang F-J, et al. The role of high high-sensitivity C-reactive protein levels at admission on poor prognosis after acute ischemic stroke[J]. The International Journal of Neuroscience, 2019, 129(5): 423–429.

[26] Wu Q, Cui J, Xie Y, et al. Outcomes of Ischemic Stroke and Associated Factors Among Elderly Patients With Large-Artery Atherosclerosis: A Hospital-Based Follow-Up Study in China[J]. Frontiers in Neurology, 2021, 12: 642426.

[27] Tan L M, Wang L, Chen J-J, et al. Diagnostic performance of bone metabolic indexes for the detection of stroke [J]. Saudi Medical Journal, 2017, 38(1): 30–35.

[28] Uehara T, Ohara T, Minematsu K, et al. Predictors of Stroke Events in Patients with Transient Ischemic Attack Attributable to Intracranial Stenotic Lesions[J]. Internal Medicine (Tokyo, Japan), 2018, 57(3): 295–300.

[29] Liu Ning, Xu Jianke, Zhang Hongyang, et al. Correlation between serum cholesterol and natural killer cells in peripheral blood in patients with acute cerebral infarction of atherosclerotic type [J]. Chinese Clinical Research, 2019, 32 (12): 1656 – 1658

[30] Shen Xueyang. Study on the correlation between residual cholesterol and carotid plaque in patients with atherosclerotic ischemic stroke [D]. Lanzhou University, 2022

[31] Zhai Qijin. Study on the correlation between trimethylamine oxide and prognosis of cerebrovascular diseases [D]. Southern Medical University, 2020.

[32] Yuan S, Tang B, Zheng J, et al. Circulating Lipoprotein Lipids, Apolipoproteins and Ischemic Stroke[J]. Annals of Neurology, 2020, 88(6): 1229–1236.

[33] Yang C, Zhang J, Liu C, et al. Comparison of the risk factors of hemorrhagic transformation between large artery atherosclerosis stroke and cardioembolism after intravenous thrombolysis[J]. Clinical Neurology and Neurosurgery, 2020, 196: 106032.

[34] Meagher E A, Barry O P, Burke A, et al. Alcohol-induced generation of lipid peroxidation products in humans[J]. The Journal of Clinical Investigation, 1999, 104(6): 805–813.

[35] Wu D, Cederbaum A I. Alcohol, oxidative stress, and free radical damage[J]. Alcohol Research & Health: The Journal of the National Institute on Alcohol Abuse and Alcoholism, 2003, 27(4): 277–284.

[36] Roberto M, Patel R R, Bajo M. Ethanol and Cytokines in the Central Nervous System[J]. Handbook of Experimental Pharmacology, 2018, 248: 397–431.

[37] Qin L, He J, Hanes R N, et al. Increased systemic and brain cytokine production and neuroinflammation by endotoxin following ethanol treatment [J]. Journal of Neuroinflammation, 2008, 5: 10.

[38] Arenillas J F, Alvarez-Sabín J. Basic mechanisms in intracranial large-artery atherosclerosis: advances and challenges[J]. Cerebrovascular Diseases (Basel, Switzerland), 2005, 20 Suppl 2: 75–83.

[39] Zafar A. Risk factors, infarct patterns and outcome differ between anterior and posterior circulation strokes attributed to intracranial large artery atherosclerotic steno-occlusive disease[J]. Clinical Neurology and Neurosurgery, 2022, 221: 107442.

[40] Qin X-D, Yang T-Q, Zeng J-H, et al. Overexpression of mitogen-activated protein kinase phosphatase-1 in endothelial cells reduces blood-brain barrier injury in a mouse model of ischemic stroke[J]. Neural Regeneration Research, 2023, 18(8): 1743–1749.

[41] Mechtouff L, Rascle L, Crespy V, et al. A narrative review of the pathophysiology of ischemic stroke in carotid plaques: a distinction versus a compromise between hemodynamic and embolic mechanism[J]. Annals of Translational Medicine, 2021, 9(14): 1208.