Pathophysiology of Ischemic Stroke: Noncoding RNA Role in Oxidative Stress

Abstract

Stroke is a neurological disease that causes significant disability and death worldwide. Ischemic stroke accounts for 75% of all strokes. The pathophysiological processes underlying ischemic stroke include oxidative stress, the toxicity of excitatory amino acids, ion disorder, enhanced apoptosis, and inflammation. Noncoding RNAs (ncRNAs) may have a vital role in regulating the pathophysiological processes of ischemic stroke, as confirmed by the altered expression of ncRNAs in blood samples from acute ischemic stroke patients, animal models, and oxygen-glucose-deprived (OGD) cell models. Due to specific changes in expression, ncRNAs can potentially be biomarkers for the diagnosis, treatment, and prognosis of ischemic stroke. As an important brain cell component, glial cells mediate the occurrence and progression of oxidative stress after ischemic stroke, and ncRNAs are an irreplaceable part of this mechanism. This review highlights the impact of ncRNAs in the oxidative stress process of ischemic stroke. It focuses on specific ncRNAs that underlie the pathophysiology of ischemic stroke and have potential as diagnostic biomarkers and therapeutic targets.

Role of histone deacetylases and sirtuins in the ischaemic stroke: a protocol for a systematic review and meta-analysis of animal studies

“…and alleviate neurotoxicity, specifically in the tissue surrounding the infarction core, known as the ischaemic penumbra. 6 Given the multifactorial nature of ischaemic brain tissue pathology, 7 previous attempts at clinical trials have been largely unsuccessful due to the interference of these treatments with vital physiological processes, as well as targeting pathological events. 8 9 Therefore, recognising these specific pathological and neuroprotective elements of the neurovascular unit can provide novel therapeutic approaches for ischaemic stroke.…”

Exploring Research Trend and Hotspots on Oxidative Stress in Ischemic Stroke (2001–2022): Insights from Bibliometric

“…Inhibition of ferroptosis has been shown to be effective in alleviating cerebral ischemia-reperfusion injury [48,49,50]. It is worth mentioning that non-coding RNAs have been expanded to understand the epigenetic regulation of cerebral ischemia-reperfusion injury by regulating genes associated with oxidative stress [51,52]. As mentioned above, the pathological and regulatory mechanisms associated with oxidative stress in reperfusion injury has not been fully explored, and there is still enough room for research.…”

Mechanisms of Mitochondrial Oxidative Stress in Brain Injury: From Pathophysiology to Therapeutics

“…One such target in surfacing research is the mitochondria. This focus largely stems from knowledge of (1) compensatory brain dysfunction and neuronal cell death in the ischemic stage and (2) enhancement of brain damage in the reperfusion stage (from overproduction of reactive oxygen species), both secondary to oxidative stress [64].…”