Evidence map›Paper›PMID 36618263›Full record

ArticleMolecular therapy. Nucleic acids2023

CDR1as regulates α-synuclein-mediated ischemic brain damage by controlling miR-7 availability.

Suresh L Mehta, Anil K Chokkalla, Saivenkateshkomal Bathula, Vijay Arruri, Bharath Chelluboina, Raghu Vemuganti

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Dual-functional nanoplatform for simultaneous degradation of circRNAJournal of Zhejiang University. Science. B · 2026
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  12. Loss of Epitranscriptomic Modification NTranslational stroke research · 2025
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  15. Article
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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

6 authors at 2 institutions in 1 country.

Suresh L MehtaDepartment of Neurological Surgery, University of Wisconsin-Madison, Madison, WI 53792, USA.
Anil K ChokkallaDepartment of Neurological Surgery, University of Wisconsin-Madison, Madison, WI 53792, USA.
Saivenkateshkomal BathulaDepartment of Neurological Surgery, University of Wisconsin-Madison, Madison, WI 53792, USA.
Vijay ArruriDepartment of Neurological Surgery, University of Wisconsin-Madison, Madison, WI 53792, USA.
Bharath ChelluboinaDepartment of Neurological Surgery, University of Wisconsin-Madison, Madison, WI 53792, USA.
Raghu VemugantiDepartment of Neurological Surgery, University of Wisconsin-Madison, Madison, WI 53792, USA.
University of Wisconsin–Madison · USNeurological Surgery · US

Funding

Role of RNAs in post-stroke brain damageR35NS132184 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI Raghu VEMUGANTI · 2023 to 2026
$4.1M
DNA hydroxymethylation and post stroke brain damageR01NS109459 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI VEMUGANTI, RAGHU · 2018 to 2022
$2.1M
BLRD VA IK6 BX005690NINDS NIH HHS R01 NS109459NINDS NIH HHS R35 NS132184
6 · The paper itself

Abstract

Transient focal ischemia decreased microRNA-7 (miR-7) levels, leading to derepression of its major target α-synuclein (α-Syn) that promotes secondary brain damage. Circular RNA CDR1as is known to regulate miR-7 abundance and function. Hence, we currently evaluated its functional significance after focal ischemia. Transient middle cerebral artery occlusion (MCAO) in adult mice significantly downregulated both CDR1as and miR-7 levels in the peri-infarct cortex between 3 and 72 h of reperfusion. Interestingly, neither pri-miR-7a nor 7b was altered in the ischemic brain. Intracerebral injection of an AAV9 vector containing a CDR1as gene significantly increased CDR1as levels by 21 days that persisted up to 4 months without inducing any observable toxicity in both sham and MCAO groups. Following transient MCAO, there was a significant increase in miR-7 levels and CDR1as binding to Ago2/miR-7 in the peri-infarct cortex of AAV9-CDR1as cohort compared with AAV9-Control cohort at 1 day of reperfusion. CDR1as overexpression significantly suppressed post-stroke α-Syn protein induction, promoted motor function recovery, decreased infarct size, and curtailed the markers of apoptosis, autophagy mitochondrial fragmentation, and inflammation in the post-stroke brain compared with AAV9-Control-treated cohort. Overall, our findings imply that CDR1as reconstitution is neuroprotective after stroke, probably by protecting miR-7 and preventing α-Syn-mediated neuronal death.

Indexed as

ischemiamotor function recoveryMT: Noncoding RNAspathological changesα-synuclein

Identifiers

PMID36618263
PMCPMC9800254
OpenAlexW4312083284

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.