Evidence map›Paper›PMID 38647405›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Alleviating Recombinant Tissue Plasminogen Activator-induced Hemorrhagic Transformation in Ischemic Stroke via Targeted Delivery of a Ferroptosis Inhibitor.

Yan-Qin Geng, Li-Na Qiu, Yuan-Qiu Cheng, Juan-Juan Li, Yi-Lin Ma, Cheng-Cheng Zhao, Ying Cai, Xue-Bin Zhang, Jieli Chen, Yu-Chen Pan and 4 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
9.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Yan-Qin GengSchool of Medicine, Nankai University, Tianjin, 300071, China.ORCID 0000-0001-7969-1534
Li-Na QiuDepartment of Neurology, Tianjin Huanhu Hospital, Tianjin, 300350, China.
Yuan-Qiu ChengCollege of Chemistry, State Key Laboratory of Elemento-Organic Chemistry, Key Laboratory of Functional Polymer Materials (Ministry of Education), Frontiers Science Center for New Organic Matter, Collaborative Innovation Center of Chemical Science and Engineering (Tianjin), Nankai University, Tianjin, 300071, China.ORCID 0000-0002-6012-1416
Juan-Juan LiCollege of Chemistry and Environmental Science, Key Laboratory of Medicinal Chemistry and Molecular Diagnosis (Ministry of Education), Key Laboratory of Chemical Biology of Hebei Province, Hebei University, Baoding, 071002, China.
Yi-Lin MaClinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300071, China.
Cheng-Cheng ZhaoClinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300071, China.
Ying CaiTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, 300350, China.
Xue-Bin ZhangDepartment of Pathology, Tianjin Huanhu Hospital, Tianjin, 300350, China.
Jieli ChenTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, 300350, China.
Yu-Chen PanCollege of Chemistry, State Key Laboratory of Elemento-Organic Chemistry, Key Laboratory of Functional Polymer Materials (Ministry of Education), Frontiers Science Center for New Organic Matter, Collaborative Innovation Center of Chemical Science and Engineering (Tianjin), Nankai University, Tianjin, 300071, China.
Ke-Rang WangCollege of Chemistry and Environmental Science, Key Laboratory of Medicinal Chemistry and Molecular Diagnosis (Ministry of Education), Key Laboratory of Chemical Biology of Hebei Province, Hebei University, Baoding, 071002, China.
Xiu-Hua YaoTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, 300350, China.
Dong-Sheng GuoCollege of Chemistry, State Key Laboratory of Elemento-Organic Chemistry, Key Laboratory of Functional Polymer Materials (Ministry of Education), Frontiers Science Center for New Organic Matter, Collaborative Innovation Center of Chemical Science and Engineering (Tianjin), Nankai University, Tianjin, 300071, China.ORCID 0000-0002-0765-5427
Jia-Ling WuSchool of Medicine, Nankai University, Tianjin, 300071, China.
Nankai University · CNTianjin Huanhu Hospital · CNHebei University · CNTianjin Medical University · CN

Funding

National Key Clinical Specialty Discipline Construction Program of China TJYXZDXK-052BNational Natural Science Foundation of China 82071316National Natural Science Foundation of China 82371320National Natural Science Foundation of China U20A20259Tianjin Health Science and Technology Project TJWJ2023QN056
6 · The paper itself

Abstract

Intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) is the primary treatment for ischemic stroke. However, rtPA treatment can substantially increase blood-brain barrier (BBB) permeability and susceptibility to hemorrhagic transformation. Herein, the mechanism underlying the side effects of rtPA treatment is investigated and demonstrated that ferroptosis plays an important role. The ferroptosis inhibitor, liproxstatin-1 (Lip) is proposed to alleviate the side effects. A well-designed macrocyclic carrier, glucose-modified azocalix[4]arene (GluAC4A), is prepared to deliver Lip to the ischemic site. GluAC4A bound tightly to Lip and markedly improved its solubility. Glucose, modified at the upper rim of GluAC4A, imparts BBB targeting to the drug delivery system owing to the presence of glucose transporter 1 on the BBB surface. The responsiveness of GluAC4A to hypoxia due to the presence of azo groups enabled the targeted release of Lip at the ischemic site. GluAC4A successfully improved drug accumulation in the brain, and Lip@GluAC4A significantly reduced ferroptosis, BBB leakage, and neurological deficits induced by rtPA in vivo. These findings deepen the understanding of the side effects of rtPA treatment and provide a novel strategy for their effective mitigation, which is of great significance for the treatment and prognosis of patients with ischemic stroke.

Indexed as

Disease Models, AnimalDrug Delivery SystemsFerroptosisIschemic StrokeTissue Plasminogen ActivatorAnimalsBlood-Brain BarrierMaleMiceQuinoxalinesSpiro Compoundsliproxstatin-1QuinoxalinesSpiro CompoundsTissue Plasminogen Activatordrug deliveryferroptosisischemic strokemacrocyclic receptorsupramolecular materials

Identifiers

PMID38647405
PMCPMC11199968
OpenAlexW4395000300

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.