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An eNOS-like nanomaterial for specific reversal of cerebral ischemia-reperfusion injury
by
Xiang, Yuting
, Xiong, Tingli
, Wang, Jue
, Shi, Xiaojing
, Li, Ruishi
, Zheng, Wenxuan
, Yang, Yongqi
, Huang, Qiong
, Wang, Shuya
, Chen, Qiaohui
, Ai, Kelong
, Chen, Wensheng
in
13/1
/ 13/2
/ 13/31
/ 13/51
/ 14/28
/ 14/34
/ 38/77
/ 38/91
/ 631/154/152
/ 631/61/350
/ 631/61/350/354
/ 64/86
/ 692/699/375/3183
/ 82/80
/ Adsorption
/ Animals
/ Blood-brain barrier
/ Blood-Brain Barrier - drug effects
/ Blood-Brain Barrier - metabolism
/ Brain - drug effects
/ Brain - metabolism
/ Brain - pathology
/ Brain Ischemia - drug therapy
/ Brain Ischemia - metabolism
/ Calcium (mitochondrial)
/ Cerebrovascular diseases
/ Damage
/ Defects
/ Disease Models, Animal
/ Disulfides - chemistry
/ Endoplasmic reticulum
/ Endoplasmic Reticulum Stress - drug effects
/ Humanities and Social Sciences
/ Humans
/ Injuries
/ Ischemia
/ Kinases
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Mitochondria - drug effects
/ Mitochondria - metabolism
/ Mitochondrial DNA
/ Molybdenum disulfide
/ multidisciplinary
/ Nanomaterials
/ Nanostructures - chemistry
/ Nitric oxide
/ Nitric Oxide - metabolism
/ Nitric Oxide Donors - chemistry
/ Nitric Oxide Donors - pharmacology
/ Nitric Oxide Synthase Type III - chemistry
/ Nitric Oxide Synthase Type III - metabolism
/ Oxidative stress
/ Reactive oxygen species
/ Reactive Oxygen Species - metabolism
/ Reperfusion
/ Reperfusion Injury - drug therapy
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Science
/ Science (multidisciplinary)
/ Vascular diseases
2025
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An eNOS-like nanomaterial for specific reversal of cerebral ischemia-reperfusion injury
by
Xiang, Yuting
, Xiong, Tingli
, Wang, Jue
, Shi, Xiaojing
, Li, Ruishi
, Zheng, Wenxuan
, Yang, Yongqi
, Huang, Qiong
, Wang, Shuya
, Chen, Qiaohui
, Ai, Kelong
, Chen, Wensheng
in
13/1
/ 13/2
/ 13/31
/ 13/51
/ 14/28
/ 14/34
/ 38/77
/ 38/91
/ 631/154/152
/ 631/61/350
/ 631/61/350/354
/ 64/86
/ 692/699/375/3183
/ 82/80
/ Adsorption
/ Animals
/ Blood-brain barrier
/ Blood-Brain Barrier - drug effects
/ Blood-Brain Barrier - metabolism
/ Brain - drug effects
/ Brain - metabolism
/ Brain - pathology
/ Brain Ischemia - drug therapy
/ Brain Ischemia - metabolism
/ Calcium (mitochondrial)
/ Cerebrovascular diseases
/ Damage
/ Defects
/ Disease Models, Animal
/ Disulfides - chemistry
/ Endoplasmic reticulum
/ Endoplasmic Reticulum Stress - drug effects
/ Humanities and Social Sciences
/ Humans
/ Injuries
/ Ischemia
/ Kinases
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Mitochondria - drug effects
/ Mitochondria - metabolism
/ Mitochondrial DNA
/ Molybdenum disulfide
/ multidisciplinary
/ Nanomaterials
/ Nanostructures - chemistry
/ Nitric oxide
/ Nitric Oxide - metabolism
/ Nitric Oxide Donors - chemistry
/ Nitric Oxide Donors - pharmacology
/ Nitric Oxide Synthase Type III - chemistry
/ Nitric Oxide Synthase Type III - metabolism
/ Oxidative stress
/ Reactive oxygen species
/ Reactive Oxygen Species - metabolism
/ Reperfusion
/ Reperfusion Injury - drug therapy
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Science
/ Science (multidisciplinary)
/ Vascular diseases
2025
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An eNOS-like nanomaterial for specific reversal of cerebral ischemia-reperfusion injury
by
Xiang, Yuting
, Xiong, Tingli
, Wang, Jue
, Shi, Xiaojing
, Li, Ruishi
, Zheng, Wenxuan
, Yang, Yongqi
, Huang, Qiong
, Wang, Shuya
, Chen, Qiaohui
, Ai, Kelong
, Chen, Wensheng
in
13/1
/ 13/2
/ 13/31
/ 13/51
/ 14/28
/ 14/34
/ 38/77
/ 38/91
/ 631/154/152
/ 631/61/350
/ 631/61/350/354
/ 64/86
/ 692/699/375/3183
/ 82/80
/ Adsorption
/ Animals
/ Blood-brain barrier
/ Blood-Brain Barrier - drug effects
/ Blood-Brain Barrier - metabolism
/ Brain - drug effects
/ Brain - metabolism
/ Brain - pathology
/ Brain Ischemia - drug therapy
/ Brain Ischemia - metabolism
/ Calcium (mitochondrial)
/ Cerebrovascular diseases
/ Damage
/ Defects
/ Disease Models, Animal
/ Disulfides - chemistry
/ Endoplasmic reticulum
/ Endoplasmic Reticulum Stress - drug effects
/ Humanities and Social Sciences
/ Humans
/ Injuries
/ Ischemia
/ Kinases
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Mitochondria - drug effects
/ Mitochondria - metabolism
/ Mitochondrial DNA
/ Molybdenum disulfide
/ multidisciplinary
/ Nanomaterials
/ Nanostructures - chemistry
/ Nitric oxide
/ Nitric Oxide - metabolism
/ Nitric Oxide Donors - chemistry
/ Nitric Oxide Donors - pharmacology
/ Nitric Oxide Synthase Type III - chemistry
/ Nitric Oxide Synthase Type III - metabolism
/ Oxidative stress
/ Reactive oxygen species
/ Reactive Oxygen Species - metabolism
/ Reperfusion
/ Reperfusion Injury - drug therapy
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Science
/ Science (multidisciplinary)
/ Vascular diseases
2025
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An eNOS-like nanomaterial for specific reversal of cerebral ischemia-reperfusion injury
Journal Article
An eNOS-like nanomaterial for specific reversal of cerebral ischemia-reperfusion injury
2025
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Overview
The protective role of NO has been widely verified in cerebrovascular diseases. However, the beneficial effects of NO depend on its concentration and reactive oxygen species (ROS) level, which makes current NO donors face great difficulties in treating cerebral ischemia-reperfusion injury (CIRI). Here, a tailored MoS
2
-based NO donor (MSNO) was constructed with defect-rich MoS
2
, in which the abundant S edge sites in the defects form -SNO, and the Mo sites can also bind NO to form Mo-NO. Combined with MSNO’s own strong ability to eliminate ROS, MSNO could provide pure NO at suitable concentrations like eNOS and avoid the generation of highly toxic ONOO
-
. After intravenous injection, MSNO with suitable nano-size could penetrate the blood-brain barrier of ischemia-reperfusion injured brain tissue, and effectively treat CIRI through multiple effects: inhibiting calcium overload, alleviating mitochondrial damage and endoplasmic reticulum stress, and inhibiting the inflammatory storm.
Nitric oxide in known to have a protective effect in cerebrovascular disease. Here, the authors report on MoS
2
an eNOS mimetic which releases NO while avoiding toxic ONOO
-
production, demonstrating therapeutic effects in inhibiting several damage pathways in cerebral ischemia-reperfusion injury.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/2
/ 13/31
/ 13/51
/ 14/28
/ 14/34
/ 38/77
/ 38/91
/ 64/86
/ 82/80
/ Animals
/ Blood-Brain Barrier - drug effects
/ Blood-Brain Barrier - metabolism
/ Brain Ischemia - drug therapy
/ Damage
/ Defects
/ Endoplasmic Reticulum Stress - drug effects
/ Humanities and Social Sciences
/ Humans
/ Injuries
/ Ischemia
/ Kinases
/ Male
/ Mice
/ Nitric Oxide Donors - chemistry
/ Nitric Oxide Donors - pharmacology
/ Nitric Oxide Synthase Type III - chemistry
/ Nitric Oxide Synthase Type III - metabolism
/ Reactive Oxygen Species - metabolism
/ Reperfusion Injury - drug therapy
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Science
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