Evidence map›Paper›PMID 34977035›Full record

ArticleFrontiers in cell and developmental biology2021

Midkine Prevents Calcification of Aortic Valve Interstitial Cells

Qian Zhou, Hong Cao, Xiaoyi Hang, Huamin Liang, Miaomiao Zhu, Yixian Fan, Jiawei Shi, Nianguo Dong, Ximiao He

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Midkine-A novel player in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  5. 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 2 institutions in 1 country.

Qian ZhouDepartment of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hong CaoDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiaoyi HangDepartment of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huamin LiangDepartment of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Miaomiao ZhuDepartment of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yixian FanDepartment of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jiawei ShiDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Nianguo DongDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ximiao HeDepartment of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcified aortic valve disease (CAVD), the most common valvular heart disease, lacks pharmaceutical treatment options because its pathogenesis remains unclear. This disease with a complex macroenvironment characterizes notable cellular heterogeneity. Therefore, a comprehensive understanding of cellular diversity and cell-to-cell communication are essential for elucidating the mechanisms driving CAVD progression and developing therapeutic targets. In this study, we used single-cell RNA sequencing (scRNA-seq) analysis to describe the comprehensive transcriptomic landscape and cell-to-cell interactions. The transitional valvular endothelial cells (tVECs), an intermediate state during the endothelial-to-mesenchymal transition (EndMT), could be a target to interfere with EndMT progression. Moreover, matrix valvular interstitial cells (mVICs) with high expression of midkine (MDK) interact with activated valvular interstitial cells (aVICs) and compliment-activated valvular interstitial cells (cVICs) through the MK pathway. Then, MDK inhibited calcification of VICs that calcification was validated by Alizarin Red S staining, real-time quantitative polymerase chain reaction (RT-qPCR), and Western blotting assays

Indexed as

CAVDcell communicationmidkine (MDK)scRNA-seqVICs’ calcification

Identifiers

PMID34977035
PMCPMC8714929
OpenAlexW4200060551

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.