Epigenetic Mechanisms of Ischemic Stroke

Uzdensky, Anatoly B.; Demyanenko, Svetlana

doi:10.1134/s1990747819040093

Cited by 3 publications

(2 citation statements)

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“…Numerous studies have suggested that insulin sensitivity inversely correlates with intracellular calcium and disturbed calcium homeostasis contributes to vascular dysfunction (Li 2015). Stroke is the major neurophysiological deficits, as a consequence of imbalance or inhibition in blood supply to the brain, resulting in loss of neurological function due to hemorrhage or ischemia-induced neuronal cell death (Uzdensky and Demyanenko 2019). Pathophysiology of stroke has complex involvement of various mechanism including loss of calcium homeostasis, glucotoxicity, lactic acidosis, excitotoxicity, free radical-mediated toxicity, cytokine-mediated cytotoxicity, complement activation, disruption of integrity of blood-brain barrier (BBB), malfunctioning of astrocytes, NMDA activation, infiltration of inflammatory mediators, and decreases in antioxidant levels (Jha et al 2019).…”

Section: Introductionmentioning

confidence: 99%

Efonidipine Exerts Cerebroprotective Effect by Down-regulation of TGF-β/SMAD-2-Dependent Signaling Pathway in Diabetic Rats

et al. 2021

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Calcium overload and hyperglycemia are risks of stroke onset in diabetics. Our study was designed to elucidate the beneficial role of calcium channel blockers by targeting voltage-gated calcium channels in diabetes-associated cerebrovascular complications. Diabetes was induced using the neonatal streptozotocin rat model. After confirmation of diabetes, middle cerebral artery occlusion (MCAO) was carried out. The pre-treatment with 1 mg/kg/day efonidipine was administered for the period of 4 weeks. After 24 h of ischemic induction surgery, the neurological score was determined, and blood was collected for determination of biochemical parameters. Treatment with efonidipine showed a significant reduction in post-ischemic brain infract volume, brain hemisphere weight difference, neurological score, Na + -K + ATPase activity, serum CK-MB, and LDH levels in normoglycemic and hyperglycemic MCAO-induced animals. While no significant changes in glucose and lipid levels were observed by treatment, efonidipine significantly decreased the levels of malondialdehyde, acetylcholine esterase, and nitrite levels and increased the levels of antioxidant markers in both normoglycemic and hyperglycemic MCAO animals. TGF-β and VEGF were found to be down-regulated after treatment with efonidipine in gene expression study. In conclusion, the study data supports the cerebroprotective role of efonidipine in diabetic animals possibly through TGF-β/SMAD-2 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Efonidipine Exerts Cerebroprotective Effect by Down-regulation of TGF-β/SMAD-2-Dependent Signaling Pathway in Diabetic Rats

et al. 2021

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“…Each of these stages is the time point of possible application of anti-stroke drugs. Many compounds tested in animal and cell models with the exception of tissue plasminogen activator (tPA) or endovascular thrombectomy [11] reduced apoptotic cell counts, increased infarction size, and improved neurological deficits after stroke [12][13][14]. However, none of these drugs have been successful in clinical trials.…”

Section: Ischemic Stroke Treatment Challengesmentioning

confidence: 99%

Histone Deacetylases and Their Isoform-Specific Inhibitors in Ischemic Stroke

2021

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Cerebral ischemia is the second leading cause of death in the world and multimodal stroke therapy is needed. The ischemic stroke generally reduces the gene expression due to suppression of acetylation of histones H3 and H4. Histone deacetylases inhibitors have been shown to be effective in protecting the brain from ischemic damage. Histone deacetylases inhibitors induce neurogenesis and angiogenesis in damaged brain areas promoting functional recovery after cerebral ischemia. However, the role of different histone deacetylases isoforms in the survival and death of brain cells after stroke is still controversial. This review aims to analyze the data on the neuroprotective activity of nonspecific and selective histone deacetylase inhibitors in ischemic stroke.

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