Evidence map›Paper›PMID 36514218›Full record

ArticleActa biochimica et biophysica Sinica2022

Deletion of large-conductance calcium-activated potassium channels promotes vascular remodelling through the CTRP7-mediated PI3K/Akt signaling pathway.

Jing Bi, Yanru Duan, Meili Wang, Chunyu He, Xiaoyue Li, Xi Zhang, Yan Tao, Yunhui Du, Huirong Liu

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

Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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

9 authors at 1 institution in 1 country.

Jing BiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Yanru DuanDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Meili WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Chunyu HeDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Xiaoyue LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Xi ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Yan TaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Yunhui DuBeijing Key Laboratory of Upper Airway Dysfunction-Related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Huirong LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The large-conductance calcium-activated potassium (BK) channel is a critical regulator and potential therapeutic target of vascular tone and architecture, and abnormal expression or dysfunction of this channel is linked to many vascular diseases. Vascular remodelling is the early pathological basis of severe vascular diseases. Delaying the progression of vascular remodelling can reduce cardiovascular events, but the pathogenesis remains unclear. To clarify the role of BK channels in vascular remodelling, we use rats with BK channel α subunit knockout (BK α

Indexed as

Large-Conductance Calcium-Activated Potassium ChannelsVascular DiseasesAnimalsBlood ProteinsHumansIntercellular Signaling Peptides and ProteinsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMatrix Metalloproteinase 2Muscle, Smooth, VascularMyocytes, Smooth MusclePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsSignal TransductionVascular RemodelingBlood ProteinsC1QTNF7 protein, humanIntercellular Signaling Peptides and ProteinsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsLarge-Conductance Calcium-Activated Potassium ChannelsMatrix Metalloproteinase 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktC1q/tumor necrosis factor-related protein 7large-conductance calcium-activated potassium channelvascular remodellingvascular smooth muscle cell

Identifiers

PMID36514218
PMCPMC10157624
OpenAlexW4311579905

What OpenQuestion holds

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LicenceCC BY-NC
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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.