Summary

Top 14 papers analyzed

Hypoxia and ischemia lead to impairment of metabolism in the brain. Cells that rely highly on oxygen and glucose such as neurons are significantly affected by oxygen and nutritional deprivation. The reduction in oxygen and substrates leads to impairment of mitochondria causing energy failure. The lack of ATP results in disturbances of metabolism and opens the mitochondrial permeability transition pore leading to apoptosis and necrosis of cells. Following restoration of oxygen and nutrients, the products of impaired metabolism cause secondary damage through generation of free radicals and excitotoxicity. To protect the brain, cells respond to hypoxia through molecular mechanisms such as upregulation of antioxidant enzymes and growth factors. Hypoxic and ischemic preconditioning render the brain tolerant to subsequent severe ischemia through upregulation of protective proteins. The protective effects involve increased production of antioxidant enzymes, heat shock proteins, growth factors and anti-apoptotic proteins. Upregulation of these pathways confers protection by reducing oxidant stress, stabilizing mitochondria, promoting cell survival signalling and inducing neurogenesis. Ischemic tolerance also involves post-translation modifications of proteins important for cell survival. Reperfusion after an ischemic period augments the injury caused by ischemia alone. Molecular oxygen supplied by reperfusion leads to an oxidative burst through generation of reactive oxygen species. Reduction of oxygen during ischemia leads to upregulation of pathways important in cell defence when oxygen is reintroduced. However, the antioxidants and cytoprotective mechanisms induced may be overwhelmed by the reactive oxygen species produced upon reperfusion. Targeting molecular mechanisms that confer endogenous neuroprotection and regulate cell death and survival signalling provide promising therapeutic strategies against ischemic brain injury. Treatment approaches such as ischemic preconditioning, hypothermia and pharmacological agents target these mechanisms to render the brain tolerant to ischemia and reperfusion injury. An improved understanding of the molecular biology of ischemic injury and protection will facilitate development of better therapeutic interventions for stroke.

Knockdown of FOXO4 promotes cell proliferation, inhibits apoptosis, and reduces oxidative stress in cerebral ischemia/reperfusion injury. This suggests FOXO4 as a potential therapeutic target for treating CIR injury.

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Trop J Pharm Res - Tropical Journal of Pharmaceutical Research

2021

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1

Oxygen is necessary for multicellular life, and the lack of oxygen can lead to injury and death in animals. In the study, researchers find that nematodes survive in a low osmotic environment during oxygen deprivation by engaging in glycogen metabolism, and this process involves a large number of genes. This research also suggests that alterations in glycogen metabolism may be responsible for the enhanced survival of mutants in the insulin-like pathway.

Published By:

Genetics

2015

Cited By:

18

The expression of long non-coding RNA MEG3 is significantly increased in ischemic stroke and is associated with poor prognosis. MEG3 may be considered as a potential intervention target and prognostic indicator for ischemic stroke.

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J atheroscler thromb - Journal of atherosclerosis and thrombosis

2020

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19

Human Wharton's jelly MSC-derived extracellular vesicles (EVs) have the potential to prevent and resolve apoptosis in neonatal brain cells following hypoxic-ischemic injury. The transfer of EV-derived let-7-5p miR appears to mediate their antiapoptotic effect.

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Cell Transplant - Cell Transplantation

2018

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51

BMP-6 protects human neural stem cells from cell death caused by oxygen and glucose deprivation (OGD), possibly through inhibiting p38 MAPK signaling pathway. This finding suggests that BMP-6 could be a potential therapeutic target for hypoxic-ischemic brain injury.

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Int j stem cell - International Journal of Stem Cells

2021

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1

Ginkgolide B activates EP4 and transactivates EGFR, leading to enhanced cell survival and inhibited apoptosis. Knockdown of EP4 prevents Ginkgolide B-mediated neuroprotective effects.

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Phytotherapy Res - Phytotherapy Research

2021

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7

Human mesenchymal stem cells (hMSCs) show promise in treating ischemic stroke, but their fate and survival after transplantation need to be monitored. This review discusses the use of superparamagnetic iron oxide (SPIO) as a contrast agent in magnetic resonance imaging to track hMSCs in ischemic environments over time.

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Brain Circ - Brain Circulation

2018

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2

Naked mole-rats have the ability to tolerate low oxygen levels without detrimental effects, unlike mice. They can substitute fructose for glucose in anaerobic metabolism, allowing them to survive under anoxic conditions.

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Cardiovasc Res - Cardiovascular Research

2017

Cited By:

0

miR-380-5p inhibits cell death in cerebral ischemia/reperfusion injury by targeting BACH1 and activating NRF2.

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Transl Neurosci - Translational Neuroscience

2021

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6

Hypoxia Inducible Factors (HIFs) are transcription factors that respond to hypoxia and control gene transcription. Their discovery revolutionized high altitude biology and has implications for various physiological functions. HIFs are highly conserved and play a crucial role in the body's response to oxygen deprivation.

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High Alt Med Biology - High Altitude Medicine & Biology

2012

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0

The text discusses the role of polymorphonuclear neutrophils (PMN) in brain injury and recovery after stroke. PMN are the first immune cells to enter the brain following stroke and can be detrimental to brain tissue. Studies have shown that inhibiting the entry of PMN into the brain can improve neurological recovery.

Published By:

Stroke

2019

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15

NRG1 signaling has been found to be neuroprotective in stroke, both in vitro and in vivo. Activation of NRG1 intracellular signaling increased neuronal survival in an in vitro model of stroke, and also improved neuronal survival in the infarcted area in an in vivo model of stroke.

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Oxidative Med Cell Longev - Oxidative Medicine and Cellular Longevity

2019

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12

Human red blood cells (RBCs) were tested to observe their morphology and death rate in different gravity fields. The results showed that RBCs can tolerate certain levels of gravity, but the death rate increased significantly as the gravity field increased.

Cited By:

0

Recent research has highlighted the dangers of breathing gases at increased tensions underwater. Breathing air limits activity due to supply problems and compressed air illness, while breathing oxygen can lead to oxygen poisoning. The use of nitrogen and oxygen mixtures can mitigate these risks, but their application is limited. The development of pressure-withstanding devices and engineering advances are key to further evolution in underwater survival.

Published By:

J Hyg - Journal of Hygiene

1948

Cited By:

8