Evidence map›Paper›PMID 40169806›Full record

ArticleScientific reports2025

Lysyl-tRNA synthetase 1 promotes atherogenesis via autophagy-related secretion and inflammation.

Kangmin Yun, Youngsik Seo, Yerim Oh, Sunghyen Kim, Hye Sun Maeng, Jin Gu Cho, Young Bae Son, Dong Ju Son, Kihwan Kwon, Sunghoon Kim and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

12 authors.

Kangmin Yun *Department of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, 119 Dandae-Ro, Dongnam-Gu, Cheonan-Si, Chungnam, 31116, South Korea.
Youngsik Seo *Department of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, 119 Dandae-Ro, Dongnam-Gu, Cheonan-Si, Chungnam, 31116, South Korea.
Yerim OhDepartment of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, 119 Dandae-Ro, Dongnam-Gu, Cheonan-Si, Chungnam, 31116, South Korea.
Sunghyen KimDepartment of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, 119 Dandae-Ro, Dongnam-Gu, Cheonan-Si, Chungnam, 31116, South Korea.
Hye Sun MaengDepartment of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, 119 Dandae-Ro, Dongnam-Gu, Cheonan-Si, Chungnam, 31116, South Korea.
Jin Gu ChoDepartment of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, 119 Dandae-Ro, Dongnam-Gu, Cheonan-Si, Chungnam, 31116, South Korea.
Young Bae SonCollege of Pharmacy, Chungbuk National University, 194-21 Osongsaengmyong 1-Ro, Osong-Eup, Heungduk-Gu, Cheongju, 28160, Chungbuk, Republic of Korea.
Dong Ju SonCollege of Pharmacy, Chungbuk National University, 194-21 Osongsaengmyong 1-Ro, Osong-Eup, Heungduk-Gu, Cheongju, 28160, Chungbuk, Republic of Korea.
Kihwan KwonDivision of Cardiology, Department of Internal Medicine, Ewha Womans University College of Medicine, Ewha Womans University Mokdong Hospital, Seoul, Republic of Korea.
Sunghoon KimDepartment of Integrative Biotechnology, Interdisciplinary Graduate Program, Medicinal Bioconvergence Research Center, Institute for Artificial Intelligence and Biomedical Research, College of Pharmacy, Yonsei University, 85 Songdogwahak-Ro, Yeonsu-Gu, Incheon, 21983, Korea.
Hanjoong JoWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Heonyong ParkDepartment of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, 119 Dandae-Ro, Dongnam-Gu, Cheonan-Si, Chungnam, 31116, South Korea. heonyong@dankook.ac.kr.

Funding

National Research Foundation of Korea NRF-2016R1D1A1B02007197National Research Foundation of Korea NRF-2021R1A3B1076605
6 · The paper itself

Abstract

Lysyl-tRNA synthetase 1 (KARS1), an aminoacyl-tRNA synthetase, was recently identified as a secreted pro-inflammatory agent. However, the vascular secretion and functions of KARS1 have not been characterized. This study investigated the secretion mechanisms of KARS1 and explored its functional roles in vascular biology. We found that KARS1 expression was upregulated by oscillatory shear stress, an atherogenic factor, suggesting the presence of free KARS1 dissociated from aminoacyl-tRNA synthetase complexes. Moreover, in the presence of Ca

Indexed as

AtherosclerosisAutophagyInflammationLysine-tRNA LigaseAnimalsEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsMicePlaque, AtheroscleroticSignal TransductionLysine-tRNA LigaseCell apoptosisKARS1Laminar shear stressOscillatory shear stressSecretory autophagyVessel alteration

Identifiers

PMID40169806
PMCPMC11961584

What OpenQuestion holds

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Registered trials

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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.