Evidence map›Paper›PMID 28698384›Full record

ArticleThe Journal of biological chemistry2017

Palmitic acid dysregulates the Hippo-YAP pathway and inhibits angiogenesis by inducing mitochondrial damage and activating the cytosolic DNA sensor cGAS-STING-IRF3 signaling mechanism.

Liangshuai Yuan, Yun Mao, Wei Luo, Weiwei Wu, Hao Xu, Xing Li Wang, Ying H Shen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

91 citing papers in PubMed, 163 citations in OpenAlex.

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  13. Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025
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31 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Liangshuai YuanFrom the Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research.
Yun MaoFrom the Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research.
Wei LuoFrom the Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research.
Weiwei WuFrom the Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research.
Hao XuFrom the Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research.
Xing Li WangFrom the Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research, xingliwang@sdu.edu.cn.
Ying H Shenthe Qilu Hospital of Shandong University, Jinan 250012, China, hyshen@bcm.edu.
Qilu Hospital of Shandong University · CNBaylor College of Medicine · US

Funding

Targeting ER Stress To Treat Aortic Aneurysms and DissectionsR01HL131980 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI LEMAIRE, SCOTT A, SHEN, YING H · 2016 to 2019
$1.7M
Mitochondrial Damage-Induced Necroptotic Cell Death in SporadicAscending Thoracic Aortic Aneurysms and DissectionsR01HL143359 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI LEMAIRE, SCOTT A, SHEN, YING H · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL131980
6 · The paper itself

Abstract

Impaired angiogenesis and wound healing carry significant morbidity and mortality in diabetic patients. Metabolic stress from hyperglycemia and elevated free fatty acids have been shown to inhibit endothelial angiogenesis. However, the underlying mechanisms remain poorly understood. In this study, we show that dysregulation of the Hippo-Yes-associated protein (YAP) pathway, an important signaling mechanism in regulating tissue repair and regeneration, underlies palmitic acid (PA)-induced inhibition of endothelial angiogenesis. PA inhibited endothelial cell proliferation, migration, and tube formation, which were associated with increased expression of mammalian Ste20-like kinases 1 (MST1), YAP phosphorylation/inactivation, and nuclear exclusion. Overexpression of YAP or knockdown of MST1 prevented PA-induced inhibition of angiogenesis. When searching upstream signaling mechanisms, we found that PA dysregulated the Hippo-YAP pathway by inducing mitochondrial damage. PA treatment induced mitochondrial DNA (mtDNA) release to cytosol, and activated cytosolic DNA sensor cGAS-STING-IRF3 signaling. Activated IRF3 bound to the

Indexed as

Adaptor Proteins, Signal TransducingCell MovementCell ProliferationCells, CulturedCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDose-Response Relationship, DrugHippo Signaling PathwayHumansInterferon Regulatory Factor-3Membrane ProteinsMitochondriaNeovascularization, PathologicNucleotidyltransferasesPalmitic AcidPhosphoproteinsProtein Serine-Threonine KinasesAdaptor Proteins, Signal TransducingcGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseInterferon Regulatory Factor-3IRF3 protein, humanMembrane ProteinsNucleotidyltransferasesPalmitic AcidPhosphoproteinsProtein Serine-Threonine KinasesSTING1 protein, humanSTING ProteinTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsangiogenesisdiabetesHippo pathwayinterferon regulatory factor (IRF)mitochondrial DNA damageMST1 (mammalian sterile 20-like kinase 1)wound healingYes-associated protein (YAP)

Identifiers

PMID28698384
PMCPMC5592676
OpenAlexW2736215167

What OpenQuestion holds

Textmetadata
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.