ReviewJournal of atherosclerosis and thrombosis2017
Therapeutic Strategies to Attenuate Hemorrhagic Transformation After Tissue Plasminogen Activator Treatment for Acute Ischemic Stroke.
Review in Journal of atherosclerosis and thrombosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.
- Mortality, functional outcome, and bleeding risk after early versus delayed thrombectomy.GeroScience · 2026Pooled it
- Association between uric acid and the risk of hemorrhagic transformation in patients with acute ischemic stroke: a systematic review and meta-analysis.Frontiers in neurology · 2024Pooled it
- Safety and Efficacy of Otaplimastat in Patients with Acute Ischemic Stroke Requiring tPA (SAFE-TPA): A Multicenter, Randomized, Double-Blind, Placebo-Controlled Phase 2 Study.Annals of neurology · 2020Trial
- Adjuvant therapy with total salvianolic acid injection enhances the safety and efficacy of recombinant prourokinase in ischemic stroke by mitigating blood-brain barrier disruption.Journal of translational medicine · 2026Article
- Matrix metalloproteinase‑9 in hemorrhagic transformation after acute ischemic stroke (Review).Molecular medicine reports · 2025Review
- Untethered miniature robots for minimally invasive thrombus treatment: From bench to clinical trials.Innovation (Cambridge (Mass.)) · 2025Review
- Mechanisms of QiShenYiQi in Inhibiting Blood-Brain Barrier Damage Following Stroke: A Network Pharmacology and Experimental Study.Combinatorial chemistry & high throughput screening · 2025Article
- Alleviating Recombinant Tissue Plasminogen Activator-induced Hemorrhagic Transformation in Ischemic Stroke via Targeted Delivery of a Ferroptosis Inhibitor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Development and validation of a machine learning-based prognostic risk stratification model for acute ischemic stroke.Scientific reports · 2023Article
- Delayed revascularization in acute ischemic stroke patients.Frontiers in pharmacology · 2023Review
- Clonidine ameliorates cerebral ischemia-reperfusion injury by up-regulating the GluN3 subunits of NMDA receptor.Metabolic brain disease · 2022Article
- Predictive accuracy of an ADC map for hemorrhagic transformation in acute ischemic stroke patients after successful recanalization with endovascular therapy.Annals of translational medicine · 2022Article
- Angong Niuhuang Wan reduces hemorrhagic transformation and mortality in ischemic stroke rats with delayed thrombolysis: involvement of peroxynitrite-mediated MMP-9 activation.Chinese medicine · 2022Article
- Optimized mouse model of embolic MCAO: From cerebral blood flow to neurological outcomes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- The Quinazoline Otaplimastat (SP-8203) Reduces the Hemorrhagic Transformation and Mortality Aggravated after Delayed rtPA-Induced Thrombolysis in Cerebral Ischemia.International journal of molecular sciences · 2022Article
- Post-stroke treatment with argon preserved neurons and attenuated microglia/macrophage activation long-termly in a rat model of transient middle cerebral artery occlusion (tMCAO).Scientific reports · 2022Article
- Association of Red Blood Cell Distribution Width with Stroke Prognosis Among Patients with Small Artery Occlusion: A Hospital-Based Prospective Follow-Up Study.International journal of general medicine · 2022Article
- Cerebral edema after ischemic stroke: Pathophysiology and underlying mechanisms.Frontiers in neuroscience · 2022Review
- Macrophage Infiltration Reduces Neurodegeneration and Improves Stroke Recovery after Delayed Recanalization in Rats.Oxidative medicine and cellular longevity · 2022Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review focuses on the mechanisms and emerging concepts of stroke and therapeutic strategies for attenuating hemorrhagic transformation (HT) after tissue plasminogen activator (tPA) treatment for acute ischemic stroke (AIS). The therapeutic time window for tPA treatment has been extended. However, the patients who are eligible for tPA treatment are still ＜5% of all patients with AIS. The risk of serious or fatal symptomatic hemorrhage increases with delayed initiation of treatment. HT is thought to be caused by 1) ischemia/reperfusion injury; 2) the toxicity of tPA itself; 3) inflammation; and/or 4) remodeling factor-mediated effects. Modulation of these pathophysiologies is the basis of direct therapeutic strategies to attenuate HT after tPA treatment. Several studies have revealed that matrix metalloproteinases and free radicals are potential therapeutic targets. In addition, we have demonstrated that the inhibition of the vascular endothelial growth factor-signaling pathway and supplemental treatment with a recombinant angiopoietin-1 protein might be a promising therapeutic strategy for attenuating HT after tPA treatment through vascular protection. Moreover, single-target therapies could be insufficient for attenuating HT after tPA treatment and improving the therapeutic outcome of patients with AIS. We recently identified progranulin, which is a growth factor and a novel target molecule with multiple therapeutic effects. Progranulin might be a therapeutic target that protects the brain through suppression of vascular remodeling (vascular protection), neuroinflammation, and/or neuronal death (neuroprotection). Clinical trials which evaluate the effects of anti-VEGF drugs or PGRN-based treatment with tPA will be might worthwhile.
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Registered trials
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