Cerebral Ischemia/Reperfusion Injury and Pharmacologic Preconditioning as a Means to Reduce Stroke-induced Inflammation and Damage

Yang, Huajun; Qi, Chengxuan; Su, Fang; Shan, Wei; Guo, Anchen; Wu, Jiahao; Wang, Yongjun; You, Hong; Wang, Qun

doi:10.1007/s11064-022-03789-5

Cited by 7 publications

(4 citation statements)

References 136 publications

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“…For example, ischemic preconditioning and postconditioning have significant protective effects on ischemia-sensitive organs. Preconditioning can reduce the likelihood of ischemic heart disease or decrease damage after myocardial ischemia reperfusion 134 ; ischemic preconditioning (IPC) or transient ischemic accidents (TIAs) induce tolerance to cerebral ischemia and can reduce the severity of subsequent stroke 135 , 136 . Postconditioning, a relatively new concept, was initially identified as a low-level hypoxic stress response.…”

Section: Discussionmentioning

confidence: 99%

Current advances and future trends of hormesis in disease

Wan,

Liu,

Mai

et al. 2024

npj Aging

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Hormesis, an adaptive response, occurs when exposure to low doses of a stressor potentially induces a stimulatory effect, while higher doses may inhibit it. This phenomenon is widely observed across various organisms and stressors, significantly advancing our understanding and inspiring further exploration of the beneficial effects of toxins at doses both below and beyond traditional thresholds. This has profound implications for promoting biological regulation at the cellular level and enhancing adaptability throughout the biosphere. Therefore, conducting bibliometric analysis in this field is crucial for accurately analyzing and summarizing its current research status. The results of the bibliometric analysis reveal a steady increase in the number of publications in this field over the years. The United States emerges as the leading country in both publication and citation numbers, with the journal Dose–Response publishing the highest number of papers in this area. Calabrese E.J. is a prominent person with significant contributions and influence among authors. Through keyword co-occurrence and trend analysis, current hotspots in this field are identified, primarily focusing on the relationship between hormesis, oxidative stress, and aging. Analysis of highly cited references predicts that future research trends may center around the relationship between hormesis and stress at different doses, as well as exploring the mechanisms and applications of hormesis. In conclusion, this review aims to visually represent hormesis-related research through bibliometric methods, uncovering emerging patterns and areas of focus within the field. It provides a summary of the current research status and forecasts trends in hormesis-related research.

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Section: Discussionmentioning

confidence: 99%

Current advances and future trends of hormesis in disease

Wan,

Liu,

Mai

et al. 2024

npj Aging

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“…The latter is subsequently dismutated into hydrogen peroxide by various superoxide dismutase (SOD) isoforms. Moreover, several antioxidant enzymes, including catalase, glutathione peroxidase (GPX), and peroxiredoxin (Prx), can effectively degrade hydrogen peroxide [ 42 , 43 ].…”

Section: Oxidative Stressmentioning

confidence: 99%

“…Intracellular calcium overload increases the production of free radicals through several mechanisms: overloading mitochondrial function by disrupting the mitochondrial ETC, activating NADPH oxidase activity, activating nNOS, leading to endoplasmic reticulum stress, and inducing the release of metals, such as iron, from intracellular stores. Metals can participate in the Fenton and Haber–Weiss reaction, promoting the overall production of ROS and RNS [ 43 , 45 ] and directly inducing lipid peroxidation and depletion of antioxidants, leading to membrane damage, loss of membrane fluidity, the formation of reactive by-products—such as malondialdehyde (MDA) or 4-hydroxynonenal—and the activation of inflammatory responses. Ultimately, these processes cause cell damage and death through several mechanisms, such as necroptosis, pyroptosis, apoptosis, ferroptosis, and autophagy [ 12 , 23 , 46 ].…”

Section: Oxidative Stressmentioning

confidence: 99%

Novel Multi-Antioxidant Approach for Ischemic Stroke Therapy Targeting the Role of Oxidative Stress

Briones-Valdivieso,

Briones,

Orellana-Urzúa

et al. 2024

Biomedicines

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Stroke is a major contributor to global mortality and disability. While reperfusion is essential for preventing neuronal death in the penumbra, it also triggers cerebral ischemia-reperfusion injury, a paradoxical injury primarily caused by oxidative stress, inflammation, and blood–brain barrier disruption. An oxidative burst inflicts marked cellular damage, ranging from alterations in mitochondrial function to lipid peroxidation and the activation of intricate signalling pathways that can even lead to cell death. Thus, given the pivotal role of oxidative stress in the mechanisms of cerebral ischemia-reperfusion injury, the reinforcement of the antioxidant defence system has been proposed as a protective approach. Although this strategy has proven to be successful in experimental models, its translation into clinical practice has yielded inconsistent results. However, it should be considered that the availability of numerous antioxidant molecules with a wide range of chemical properties can affect the extent of injury; several groups of antioxidant molecules, including polyphenols, carotenoids, and vitamins, among other antioxidant compounds, can mitigate this damage by intervening in multiple signalling pathways at various stages. Multiple clinical trials have previously been conducted to evaluate these properties using melatonin, acetyl-L-carnitine, chrysanthemum extract, edaravone dexborneol, saffron, coenzyme Q10, and oleoylethanolamide, among other treatments. Therefore, multi-antioxidant therapy emerges as a promising novel therapeutic option due to the potential synergistic effect provided by the simultaneous roles of the individual compounds.

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“…I/R injury is initiated in the ischemic phase, mainly as a result of deficiency in oxygen or nutrients supply to neural cells 3 . However, when blood flow is restored during the reperfusion phase, the ischemic zone of the brain can undergo oxidative stress, inflammatory responses and disordered energy metabolism 4 , resulting in blood-brain barrier disruption, neuronal death 5 , brain edema and hemorrhaging 6 . Considering that cerebral I/R injury has been associated with motor dysfunction, cognitive impairment and even death, it is important to determine the pathological alterations underlying brain I/R.…”

Section: Introductionmentioning

confidence: 99%

Sirtuin-3 activates the mitochondrial unfolded protein response and reduces cerebral ischemia/reperfusion injury

Xiaowei,

Qian,

Dingzhou

2023

Int. J. Biol. Sci.

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Sirtuin-3 (Sirt3) deacetylates several mitochondrial proteins implicated into cerebral ischemia/reperfusion (I/R) injury. The mitochondrial unfolded protein response (UPR mt ) favors mitochondrial proteostasis during various stressors. Here, we used Sirt3 transgenic mice and a transient middle cerebral artery occlusion model to evaluate the molecular basis of Sirt3 on the UPR mt during brain post-ischemic dysfunction. The present study illustrated that Sirt3 abundance was suppressed in the brain after brain ischemic abnormalities. Overexpression of Sirt3 in vivo suppressed the infarction size and attenuated neuroinflammation after brain I/R injury. Sirt3 overexpression restored neural viability by reducing mitochondrial ROS synthesis, maintaining the mitochondrial potential and improving mitochondrial adenosine triphosphate synthesis. Sirt3 overexpression protected neuronal mitochondria against brain post-ischemic malfunction via eliciting the UPR mt by the forkhead box O3 (Foxo3)/sphingosine kinase 1 (Sphk1) pathway. Inhibiting either the UPR mt or the Foxo3/Sphk1 pathway relieved the favorable influence of Sirt3 on neural function and mitochondrial behavior. In contrast, Sphk1 overexpression was sufficient to reduce the infarction size, attenuate neuroinflammation, sustain neuronal viability and prevent mitochondrial abnormalities during brain post-ischemia dysfunction. Thus, the UPR mt protects neural viability and mitochondrial homeostasis, and the Sirt3/Foxo3/Sphk1 pathway is a promosing therapeutic candidate for ischemic stroke.

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Cerebral Ischemia/Reperfusion Injury and Pharmacologic Preconditioning as a Means to Reduce Stroke-induced Inflammation and Damage

Cited by 7 publications

References 136 publications

Current advances and future trends of hormesis in disease

Current advances and future trends of hormesis in disease

Novel Multi-Antioxidant Approach for Ischemic Stroke Therapy Targeting the Role of Oxidative Stress

Sirtuin-3 activates the mitochondrial unfolded protein response and reduces cerebral ischemia/reperfusion injury

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