Reactive nitrogen species as therapeutic targets for autophagy: implication for ischemic stroke

Feng, Jie; Chen, Xingmiao; Shen, Jiangang

doi:10.1080/14728222.2017.1281250

Cited by 37 publications

(20 citation statements)

References 177 publications

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“…Recent reports also suggest a possible role for autophagy, being presumably regulated under diverse pathological conditions including stroke. Yet, the precise role of stroke-associated autophagy is elusive with autophagy being a double-edged sword that can be either protective or harmful [50]. Autophagy, however, appears to be of no concern in CCL11-aggravated ischemic brain injury of adult mice.…”

Section: Discussionmentioning

confidence: 99%

CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age

Lieschke

Zechmeister

Haupt

et al. 2019

Cells

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CCL11 has recently been shown to differentially affect cell survival under various pathological conditions including stroke. Indeed, CCL11 promotes neuroregeneration in neonatal stroke mice. The impact of CCL11 on the adult ischemic brain, however, remains elusive. We therefore studied the effect of ectopic CCL11 on both adolescent (six-week) and adult (six-month) C57BL6 mice exposed to stroke. Intraperitoneal application of CCL11 significantly aggravated acute brain injury in adult mice but not in adolescent mice. Likewise, post-stroke neurological recovery after four weeks was significantly impaired in adult mice whilst CCL11 was present. On the contrary, CCL11 stimulated gliogenesis and neurogenesis in adolescent mice. Flow cytometry analysis of blood and brain samples revealed a modification of inflammation by CCL11 at subacute stages of the disease. In adolescent mice, CCL11 enhances microglial cell, B and T lymphocyte migration towards the brain, whereas only the number of B lymphocytes is increased in the adult brain. Finally, the CCL11 inhibitor SB297006 significantly reversed the aforementioned effects. Our study, for the first time, demonstrates CCL11 to be a key player in mediating secondary cell injury under stroke conditions. Interfering with this pathway, as shown for SB297006, might thus be an interesting approach for future stroke treatment paradigms.

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Section: Discussionmentioning

confidence: 99%

CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age

Lieschke

Zechmeister

Haupt

et al. 2019

Cells

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“…Particularly for ischemic brain injury, we concluded that the interaction of RNS, Cav-1 and MMPs could form a positive feedback loop, amplifying the impact of RNS in BBB disruption and ischemic brain injury ( Figure 1 ). Therefore, targeting the RNS/Cav-1/MMP pathway is a promising therapeutic strategy for protecting against cerebral ischemia-reperfusion injury 28 , 108 , 123 .…”

Section: Role Of Caveolin-1 In Acute Ischemic Brain Injurymentioning

confidence: 99%

Targeting RNS/caveolin-1/MMP signaling cascades to protect against cerebral ischemia-reperfusion injuries: potential application for drug discovery

Chen

et al. 2018

Acta Pharmacol Sin

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Reactive nitrogen species (RNS) play important roles in mediating cerebral ischemia-reperfusion injury. RNS activate multiple signaling pathways and participate in different cellular events in cerebral ischemia-reperfusion injury. Recent studies have indicated that caveolin-1 and matrix metalloproteinase (MMP) are important signaling molecules in the pathological process of ischemic brain injury. During cerebral ischemia-reperfusion, the production of nitric oxide (NO) and peroxynitrite (ONOO−), two representative RNS, down-regulates the expression of caveolin-1 (Cav-1) and, in turn, further activates nitric oxide synthase (NOS) to promote RNS generation. The increased RNS further induce MMP activation and mediate disruption of the blood-brain barrier (BBB), aggravating the brain damage in cerebral ischemia-reperfusion injury. Therefore, the feedback interaction among RNS/Cav-1/MMPs provides an amplified mechanism for aggravating ischemic brain damage during cerebral ischemia-reperfusion injury. Targeting the RNS/Cav-1/MMP pathway could be a promising therapeutic strategy for protecting against cerebral ischemia-reperfusion injury. In this mini-review article, we highlight the important role of the RNS/Cav-1/MMP signaling cascades in ischemic stroke injury and review the current progress of studies seeking therapeutic compounds targeting the RNS/Cav-1/MMP signaling cascades to attenuate cerebral ischemia-reperfusion injury. Several representative natural compounds, including calycosin-7-O-β-D-glucoside, baicalin, Momordica charantia polysaccharide (MCP), chlorogenic acid, lutein and lycopene, have shown potential for targeting the RNS/Cav-1/MMP signaling pathway to protect the brain in ischemic stroke. Therefore, the RNS/Cav-1/MMP pathway is an important therapeutic target in ischemic stroke treatment.

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“…PINK1/Parkin-mediated mitophagy is activated in brain damage induced by ischemia stroke; however, the underlying function is unclear [162]. Although the function of mitophagy is still unclear in stroke, it is generally accepted that the degree of mitophagy is the determinant during stroke, and physiological levels can be beneficial, while excessive or inadequate levels could be deleterious [30,163].…”

Section: Strokementioning

confidence: 99%

Role of Mitophagy in Cardiovascular Disease

Yang¹,

Li²,

Li³

et al. 2020

Aging and disease

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Cardiovascular disease is the leading cause of mortality worldwide, and mitochondrial dysfunction is the primary contributor to these disorders. Recent studies have elaborated on selective autophagy-mitophagy, which eliminates damaged and dysfunctional mitochondria, stabilizes mitochondrial structure and function, and maintains cell survival and growth. Numerous recent studies have reported that mitophagy plays an important role in the pathogenesis of various cardiovascular diseases. This review summarizes the mechanisms underlying mitophagy and advancements in studies on the role of mitophagy in cardiovascular disease.

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Reactive nitrogen species as therapeutic targets for autophagy: implication for ischemic stroke

Cited by 37 publications

References 177 publications

CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age

CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age

Targeting RNS/caveolin-1/MMP signaling cascades to protect against cerebral ischemia-reperfusion injuries: potential application for drug discovery

Role of Mitophagy in Cardiovascular Disease

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