Evidence map›Paper›PMID 34619327›Full record

ArticleFree radical biology & medicine2021

Disturbed flow-induced FAK K152 SUMOylation initiates the formation of pro-inflammation positive feedback loop by inducing reactive oxygen species production in endothelial cells.

Loka Reddy Velatooru, Rei J Abe, Masaki Imanishi, Young Jin Gi, Kyung Ae Ko, Kyung-Sun Heo, Keigi Fujiwara, Nhat-Tu Le, Sivareddy Kotla

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Focal Adhesion Kinase Variants May Contribute to Risk of Human Myelomeningocele.medRxiv : the preprint server for health sciences · 2025
    Article
  2. FAK Family Kinases: A Potential Therapeutic Target for Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023
    Review
  8. Review
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 3 institutions in 2 countries.

Loka Reddy VelatooruCenter for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, 77030, Texas, USA.
Rei J AbeCenter for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, 77030, Texas, USA.
Masaki ImanishiDepartment of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, 77030, Texas, USA.
Young Jin GiDepartment of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, 77030, Texas, USA.
Kyung Ae KoDepartment of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, 77030, Texas, USA.
Kyung-Sun HeoInstitute of Drug Research and Development, Chungnam National University, Daejeon, Republic of Korea.
Keigi FujiwaraDepartment of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, 77030, Texas, USA.
Nhat-Tu LeCenter for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, 77030, Texas, USA. Electronic address: nhle@houstonmethodist.org.
Sivareddy KotlaDepartment of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, 77030, Texas, USA. Electronic address: SKotla@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USHouston Methodist · USChungnam National University · KR

Funding

A Novel Role for MAGI1 in regulating non-canonical LATS signaling and atherosclerotic plaque formationR01HL134740 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LE, NHAT-TU · 2017 to 2021
$2.0M
NHLBI NIH HHS R01 HL134740
6 · The paper itself

Abstract

Focal adhesion kinase (FAK) activation plays a crucial role in vascular diseases. In endothelial cells, FAK activation is involved in the activation of pro-inflammatory signaling and the progression of atherosclerosis. Disturbed flow (D-flow) induces endothelial activation and senescence, but the exact role of FAK in D-flow-induced endothelial activation and senescence remains unclear. The objective of this study is to investigate the role of FAK SUMOylation in D-flow-induced endothelial activation and senescence. The results showed that D-flow induced reactive oxygen species (ROS) production via NADPH oxidase activation and activated a redox-sensitive kinase p90RSK, leading to FAK activation by upregulating FAK K152 SUMOylation and the subsequent Vav2 phosphorylation, which in turn formed a positive feedback loop by upregulating ROS production. This feedback loop played a crucial role in regulating endothelial activation and senescence. D-flow-induced endothelial activation and senescence were significantly inhibited by mutating a FAK SUMOylation site lysine152 to arginine. Collectively, we concluded that FAK K152 SUMOylation plays a key role in D-flow-induced endothelial activation and senescence by forming a positive feedback loop through ROS production.

Indexed as

Endothelial CellsSumoylationFeedbackFocal Adhesion Protein-Tyrosine KinasesHumansInflammationPhosphorylationReactive Oxygen SpeciesFocal Adhesion Protein-Tyrosine KinasesReactive Oxygen SpeciesDisturbed flowFAKp90RSKReactive oxygen speciesSUMOylation

Identifiers

PMID34619327
PMCPMC8664087
OpenAlexW3204049184

What OpenQuestion holds

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LicenceTDM
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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.