Evidence map›Paper›PMID 27470514›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

Essential Role of Smooth Muscle STIM1 in Hypertension and Cardiovascular Dysfunction.

Modar Kassan, Karima Ait-Aissa, Eman Radwan, Vishal Mali, Samuel Haddox, Mohanad Gabani, Wei Zhang, Souad Belmadani, Kaikobad Irani, Mohamed Trebak and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 58 citations in OpenAlex.

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  16. Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022
    Review
  17. Article
  18. STIM1 is a core trigger of airway smooth muscle remodeling and hyperresponsiveness in asthma.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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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

11 authors at 1 institution in 1 country.

Modar KassanFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Karima Ait-AissaFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Eman RadwanFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Vishal MaliFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Samuel HaddoxFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Mohanad GabaniFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Wei ZhangFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Souad BelmadaniFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Kaikobad IraniFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).
Mohamed TrebakFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.). matrouk@evms.edu mtrebak@hmc.psu.edu.
Khalid MatrouguiFrom the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.). matrouk@evms.edu mtrebak@hmc.psu.edu.
Tulane University · US

Funding

INTERDISCIPLINARY CARDIOVASCULAR RESEARCH FELLOWSHIPT32HL007121 · NHLBI · UNIVERSITY OF IOWA · PI LONDON, BARRY · 1985 to 2020
$15.1M
Receptor-regulated Ca2+ Entry Pathways in Smooth MuscleR01HL097111 · NHLBI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI TREBAK, MOHAMED · 2010 to 2019
$3.7M
Mechanisms of Coronary Arteriolar Dysfunction in Type 2 DiabetesR01HL095566 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI MATROUGUI, KHALID · 2010 to 2014
$1.8M
Leukotriene C4 and STIM/Orai channels in airway smooth muscle remodelingR01HL123364 · NHLBI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI TREBAK, MOHAMED · 2014 to 2017
$1.5M
Genes and miRNAs controlled by ORAI3 in cardiovascular remodelingR21AG050072 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEBECHE, DJAMEL, TREBAK, MOHAMED · 2016 to 2017
$471k
NHLBI NIH HHS R01 HL095566NHLBI NIH HHS R01 HL097111NHLBI NIH HHS R01 HL123364NHLBI NIH HHS T32 HL007121NIA NIH HHS R21 AG050072
6 · The paper itself

Abstract

objectivesChronic hypertension is the most critical risk factor for cardiovascular disease, heart failure, and stroke. APPROACH AND

resultsHere we show that wild-type mice infused with angiotensin II develop hypertension, cardiac hypertrophy, perivascular fibrosis, and endothelial dysfunction with enhanced stromal interaction molecule 1 (STIM1) expression in heart and vessels. All these pathologies were significantly blunted in mice lacking STIM1 specifically in smooth muscle (Stim1(SMC-/-)). Mechanistically, STIM1 upregulation during angiotensin II-induced hypertension was associated with enhanced endoplasmic reticulum stress, and smooth muscle STIM1 was required for endoplasmic reticulum stress-induced vascular dysfunction through transforming growth factor-β and nicotinamide adenine dinucleotide phosphate oxidase-dependent pathways. Accordingly, knockout mice for the endoplasmic reticulum stress proapoptotic transcriptional factor, CCAAT-enhancer-binding protein homologous protein (CHOP(-/-)), were resistant to hypertension-induced cardiovascular pathologies. Wild-type mice infused with angiotensin II, but not Stim1(SMC-/-) or CHOP(-/-) mice showed elevated vascular nicotinamide adenine dinucleotide phosphate oxidase activity and reduced phosphorylated endothelial nitric oxide synthase, cGMP, and nitrite levels.

conclusionsThus, smooth muscle STIM1 plays a crucial role in the development of hypertension and associated cardiovascular pathologies and represents a promising target for cardiovascular therapy.

Indexed as

Blood PressureVasodilationAngiotensin IIAnimalsCardiomegalyCyclic GMPDisease Models, AnimalDose-Response Relationship, DrugEndoplasmic Reticulum StressFibrosisGenetic Predisposition to DiseaseHypertensionMaleMice, KnockoutMuscle, Smooth, VascularMyocardiumAngiotensin IICyclic GMPDdit3 protein, mouseNADPH OxidasesNitric Oxide Synthase Type IIINitritesNos3 protein, mouseReactive Oxygen SpeciesStim1 protein, mouseStromal Interaction Molecule 1Transcription Factor CHOPTransforming Growth Factor betaVasodilator Agentscardiac hypertrophyendothelial nitric oxide synthaseER stresshypertensionnicotinamide adenine dinucleotide phosphatestromal interaction molecule 1vascular reactivity

Identifiers

PMID27470514
PMCPMC5061131
OpenAlexW2489374855

What OpenQuestion holds

Textmetadata
LicenceTDM
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.