Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): are neurologists feeling more comfortable to RESTART antiplatelet?

Girotra, Tarun; Feng, Wuwei

doi:10.21037/atm.2019.08.84

Cited by 2 publications

(2 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A much larger randomized clinical trial could investigate several remaining uncertainties about antiplatelet therapy after ICH, including whether there is an overall reduction in major vascular events after ICH of similar magnitude to that seen in patients without ICH; whether time since ICH and duration of antiplatelet therapy modify these effects; whether effects vary in other subgroups (such as lobar ICH location, which is a risk factor for ICH recurrence [eFigures 1 and 2 in Supplement 1], or other imaging features that may modify risks of recurrent ICH or ischemic stroke); and whether antiplatelet therapy is beneficial for ICH survivors without prior antithrombotic drug use or major vascular events …”

Section: Discussionmentioning

confidence: 99%

Effects of Antiplatelet Therapy After Stroke Caused by Intracerebral Hemorrhage

et al. 2021

View full text Add to dashboard Cite

IMPORTANCE The Restart or Stop Antithrombotics Randomized Trial (RESTART) found that antiplatelet therapy appeared to be safe up to 5 years after intracerebral hemorrhage (ICH) that had occurred during antithrombotic (antiplatelet or anticoagulant) therapy.OBJECTIVES To monitor adherence, increase duration of follow-up, and improve precision of estimates of the effects of antiplatelet therapy on recurrent ICH and major vascular events.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of Antiplatelet Therapy After Stroke Caused by Intracerebral Hemorrhage

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Transient ischemic attack, ischemic stroke, and hemorrhagic stroke are the common forms of cerebrovascular diseases. Of these, ischemic stroke, which accounts for over 80% of cerebrovascular diseases, remains a leading cause of disability and mortality (2). Currently, the common treatment for vascular occlusion in ischemic stroke is prompt thrombolytic therapy which consists of intravenous thrombolysis and mechanical thrombolysis (3,4).…”

Section: Introductionmentioning

confidence: 99%

LncRNA MACC1-AS1 attenuates microvascular endothelial cell injury and promotes angiogenesis under hypoxic conditions via modulating miR-6867-5p/TWIST1 in human brain microvascular endothelial cells

Yan¹,

Zhao²,

Xiao³

2020

Ann Transl Med

View full text Add to dashboard Cite

Background: Hypoxia following ischemic stroke is a common cause of brain insults. Mounting evidence suggests that long non-coding RNAs (lncRNAs) play a vital role in regulating certain physiological and pathological processes including ischemic stroke. For the first time, the present study investigated the effects and mechanism of LncRNA MACC1-AS1 on hypoxia-induced human brain microvascular endothelial cells (HBMECs).Methods: LncRNA MACC1-AS1 levels in HBMECs were detected via reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay. Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT), were detected using their respective kits. Flow cytometry and clone formation assay were performed to evaluate the effects of lncRNA MACC1-AS1 on cell apoptosis and cell proliferation respectively. Angiogenesis capacity was evaluated via tube formation assay. Transwell migration assay was performed for assessment of cell migration, Western blot assay was performed for measurement of Twist1 and VE-cadherin level, and permeability assay was performed for evaluation of the cell barrier function. The target gene was predicted via bioinformatics online tool and validated through luciferase reporter assay and RNA pull-down assay.Results: LncRNA MACC1-AS1 was downregulated in hypoxia-induced HBMECs. Overexpression of LncRNA MACC1-AS1 reduced cell apoptosis and oxidative stress, while promoting cell proliferation, migration, and angiogenesis. Moreover, LncRNA MACC1-AS1 overexpression reduced cell permeability and elevated VE-cadherin level, which contributed to maintaining cell barrier function. TWIST1 was validated as the target of miR-6867-5p which was further targeted by lncRNA MACC1-AS1. Thus, LncRNA MACC1-AS1 functions in hypoxia-induced HBMECs by regulating miR-6867-5p/TWIST1. Conclusions:In this study, we found that LncRNA MACC1-AS1 exerted a protective role in hypoxiainduced HBMECs via regulating miR-6867-5p/TWIST1, indicating a new therapeutic strategy for future ischemic stroke therapy.

show abstract

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): are neurologists feeling more comfortable to RESTART antiplatelet?

Cited by 2 publications

References 23 publications

Effects of Antiplatelet Therapy After Stroke Caused by Intracerebral Hemorrhage

Effects of Antiplatelet Therapy After Stroke Caused by Intracerebral Hemorrhage

LncRNA MACC1-AS1 attenuates microvascular endothelial cell injury and promotes angiogenesis under hypoxic conditions via modulating miR-6867-5p/TWIST1 in human brain microvascular endothelial cells

Contact Info

Product

Resources

About