Non-mitogenic fibroblast growth factor 1 protects against ischemic stroke by regulating microglia/macrophage polarization through Nrf2 and NF-κB pathways

Dordoe, Confidence; Wang, Xue; Lin, Ping; Wang, Zhengyi; Hu, Jian; Wang, Dongxue; Fang, Yani; Liang, Fei; Ye, Shasha; Zhao, Yanrong; Xiong, Ye; Yang, Yunjun; Lin, Li; Li, Xianfeng

doi:10.1016/j.neuropharm.2022.109064

Cited by 21 publications

(14 citation statements)

References 70 publications

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“… 91 In the transient MCAO model, Nrf2 proved to be essential in sevoflurane preconditioning as adeno‐associated virus (AAV)‐shNrf2‐abolished this protection. 92 A similar association was also reported in the protection afforded by tanshinol borneol ester, 23 non‐mitogenic fibroblast growth factor 1, 40 and HP‐1c, a dual Nrf2/AMP‐activated protein kinase (AMPK) activator. 93 In primary microglial cultures or BV2 cultures, the causal relationship between Nrf2 and M2 has been proven consistently, upon either OGD or lipopolysaccharide stimuli.…”

Section: Cell‐specific Role Of Nrf2 In the Acute Phasesupporting

confidence: 64%

“…Studies by our group and others consistently demonstrated the pivotal role of Nrf2 in reducing infarct volume and rescuing neuronal loss after ischemic stroke. 37 , 38 , 39 , 40 Mechanistically, sublethal ischemia in the penumbra leads to sublethal intracellular calcium accumulation, resulting in hyperpermeability of the mitochondria membrane. Apoptosis is mainly triggered by the leakage of mitochondrial content.…”

Section: Cell‐specific Role Of Nrf2 In the Acute Phasementioning

confidence: 99%

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The cell‐specific roles of Nrf2 in acute and chronic phases of ischemic stroke

Fadoul,

Ikonomovic,

Zhang

et al. 2023

CNS Neurosci Ther

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Ischemic stroke refers to the sudden loss of blood flow in a specific area of the brain. It is the fifth leading cause of mortality and the leading cause of permanent disability. The transcription factor nuclear factor erythroid 2‐related factor 2 (Nrf2) controls the production of several antioxidants and protective proteins and it has been investigated as a possible pharmaceutical target for reducing harmful oxidative events in brain ischemia. Each cell type exhibits different roles and behaviors in different phases post‐stroke, which is comprehensive yet important to understand to optimize management strategies and goals for care for stroke patients. In this review, we comprehensively summarize the protective effects of Nrf2 in experimental ischemic stroke, emphasizing the role of Nrf2 in different cell types including neurons, astrocytes, oligodendrocytes, microglia, and endothelial cells during acute and chronic phases of stroke and providing insights on the neuroprotective role of Nrf2 on each cell type throughout the long term of stroke care. We also highlight the importance of targeting Nrf2 in clinical settings while considering a variety of important factors such as age, drug dosage, delivery route, and time of administration.

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Section: Cell‐specific Role Of Nrf2 In the Acute Phasesupporting

confidence: 64%

Section: Cell‐specific Role Of Nrf2 In the Acute Phasementioning

confidence: 99%

The cell‐specific roles of Nrf2 in acute and chronic phases of ischemic stroke

Fadoul,

Ikonomovic,

Zhang

et al. 2023

CNS Neurosci Ther

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“…These findings were corroborated in in vitro experiments, indicating that nonmitogenic FGF1 holds promise as an agent against ischemic stroke. [229] The NLRP3 (NLR pyrin domain-containing 3) inflammasome serves as a crucial component in the inflammatory response following stroke. [230] Lin et al discovered that the cardiac dysfunction induced by AIS is more severe in a type 2 diabetes mice model.…”

Section: Cardiovascular Monitoring and Treatment Options After Aismentioning

confidence: 99%

“…These findings were corroborated in in vitro experiments, indicating that nonmitogenic FGF1 holds promise as an agent against ischemic stroke. [ 229 ]…”

Section: Cardiovascular Monitoring and Treatment Options After Aismentioning

confidence: 99%

Stroke Related Brain–Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms

Fan,

Cao,

et al. 2024

Advanced Science

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The emergence of acute ischemic stroke (AIS) induced cardiovascular dysfunctions as a bidirectional interaction has gained paramount importance in understanding the intricate relationship between the brain and heart. Post AIS, the ensuing cardiovascular dysfunctions encompass a spectrum of complications, including heart attack, congestive heart failure, systolic or diastolic dysfunction, arrhythmias, electrocardiographic anomalies, hemodynamic instability, cardiac arrest, among others, all of which are correlated with adverse outcomes and mortality. Mounting evidence underscores the intimate crosstalk between the heart and the brain, facilitated by intricate physiological and neurohumoral complex networks. The primary pathophysiological mechanisms contributing to these severe cardiac complications involve the hypothalamic‐pituitary‐adrenal (HPA) axis, sympathetic and parasympathetic hyperactivity, immune and inflammatory responses, and gut dysbiosis, collectively shaping the stroke‐related brain–heart axis. Ongoing research endeavors are concentrated on devising strategies to prevent AIS‐induced cardiovascular dysfunctions. Notably, labetalol, nicardipine, and nitroprusside are recommended for hypertension control, while β‐blockers are employed to avert chronic remodeling and address arrhythmias. However, despite these therapeutic interventions, therapeutic targets remain elusive, necessitating further investigations into this complex challenge. This review aims to delineate the state‐of‐the‐art pathophysiological mechanisms in AIS through preclinical and clinical research, unraveling their intricate interplay within the brain–heart axis, and offering pragmatic suggestions for managing AIS‐induced cardiovascular dysfunctions.

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“…The nuclear transcription Nrf2 is a key molecule that mitigates the effects of oxidative stress in cells [ 16 ]. Translocation of Nrf2 from cytosol to nucleus promotes the expression of downstream antioxidant genes, including heme oxygenase-1 (HO-1), and enhances the activity of antioxidant-related enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH), to scavenge excessive ROS [ 17 , 18 ]. However, oxygen and glucose deprivation in ischemic stroke results in excessive ROS, and then Nrf2 is activated and released from keap1 into the nucleus to bind to antioxidant response elements (ARE) in order to regulate the expression levels of several antioxidant enzymes; on the other hand, Nrf2-downstream proteins can mitigate the deleterious effects of oxidants produced in excess during reoxygenation [ 16 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effect of Polyphenol Extracts from Terminalia chebula Retz. against Cerebral Ischemia-Reperfusion Injury

et al. 2022

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Current therapies for ischemic stroke are insufficient due to the lack of specific drugs. This study aimed to investigate the protective activity of polyphenol extracts from Terminalia chebula against cerebral ischemia-reperfusion induced damage. Polyphenols of ethyl acetate and n-butanol fractions were extracted from T. chebula. BV2 microglial cells exposed to oxygen-glucose deprivation/reoxygenation and mice subjected to middle cerebral artery occlusion/reperfusion were treated by TPE and TPB. Cell viability, cell morphology, apoptosis, mitochondrial membrane potential, enzyme activity and signaling pathway related to oxidative stress were observed. We found that TPE and TPB showed strong antioxidant activity in vitro. The protective effects of TPE and TPB on cerebral ischemia-reperfusion injury were demonstrated by enhanced antioxidant enzyme activities, elevated level of the nucleus transportation of nuclear factor erythroid 2-related factor 2 and expressions of antioxidant proteins, with a simultaneous reduction in cell apoptosis and reactive oxygen species level. In conclusion, TPE and TPB exert neuroprotective effects by stimulating the Nrf2 signaling pathway, thereby inhibiting apoptosis.

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Non-mitogenic fibroblast growth factor 1 protects against ischemic stroke by regulating microglia/macrophage polarization through Nrf2 and NF-κB pathways

Cited by 21 publications

References 70 publications

The cell‐specific roles of Nrf2 in acute and chronic phases of ischemic stroke

The cell‐specific roles of Nrf2 in acute and chronic phases of ischemic stroke

Stroke Related Brain–Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms

Neuroprotective Effect of Polyphenol Extracts from Terminalia chebula Retz. against Cerebral Ischemia-Reperfusion Injury

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