Evidence map›Paper›PMID 33144524›Full record

ArticleAging2020

Smyd3-PARP16 axis accelerates unfolded protein response and vascular aging.

Di Yang, Qing Wang, Gang Wei, Jiaxue Wu, Yi Chun Zhu, Qing Zhu, Ting Ni, Xinhua Liu, Yi Zhun Zhu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  9. New insights of epigenetics in vascular and cellular senescence.Journal of translational internal medicine · 2021
    Review
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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

9 authors at 5 institutions in 2 countries.

Di YangDepartment of Pharmacology, Human Phenome Institute, School of Pharmacy, Fudan University, Shanghai, P.R. China.
Qing WangDepartment of Pharmacology, Human Phenome Institute, School of Pharmacy, Fudan University, Shanghai, P.R. China.
Gang WeiState Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, Collaborative Innovation Center of Genetics and Development, Human Phenome Institute, School of Life Sciences and Huashan Hospital, Fudan University, Shanghai, P.R. China.
Jiaxue WuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, P.R. China.
Yi Chun ZhuShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, P.R. China.
Qing ZhuSchool of Pharmacy, Nantong University, Nantong, P.R. China.
Ting NiState Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, Collaborative Innovation Center of Genetics and Development, Human Phenome Institute, School of Life Sciences and Huashan Hospital, Fudan University, Shanghai, P.R. China.
Xinhua LiuDepartment of Pharmacology, Human Phenome Institute, School of Pharmacy, Fudan University, Shanghai, P.R. China.
Yi Zhun ZhuDepartment of Pharmacology, Human Phenome Institute, School of Pharmacy, Fudan University, Shanghai, P.R. China.
Fudan University · CNMacau University of Science and Technology · MOHuashan Hospital · CNNantong University · CNState Key Laboratory of Genetic Engineering

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelial cell senescence and endoplasmic reticulum (ER) stress induced unfolded protein response (UPR) are two critical contributors to individual aging. However, whether these two biological events have crosstalk and are controlled by shared upstream regulators are largely unknown. Here, we found PARP16, a member of the Poly (ADP-ribose) polymerases family that tail-anchored ER transmembrane, was upregulated in angiotensin II (Ang II)-induced vascular aging and promoted UPR. Further, PARP16 was epigenetically upregulated by Smyd3, a histone H3 lysine 4 methyltransferase that bound to the promotor region of

Indexed as

Cellular SenescenceUnfolded Protein ResponseAngiotensin IIAnimalsAorta, ThoracicBinding SitesCells, CulturedDNA MethylationEndothelial CellsEpigenesis, GeneticGene Expression RegulationHistone-Lysine N-MethyltransferaseMaleMice, Inbred C57BLPoly(ADP-ribose) PolymerasesPromoter Regions, GeneticAngiotensin IIHistone-Lysine N-MethyltransferaseParp16 protein, ratPoly(ADP-ribose) PolymerasesSmyd3 protein, mouseangiotensin IIendoplasmic reticulumPARP16Smyd3vascular endothelial cell

Identifiers

PMID33144524
PMCPMC7695420
OpenAlexW3095771135

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.