Evidence map›Paper›PMID 27724862›Full record

ArticleBMC cardiovascular disorders2016

RhoA/rock signaling mediates peroxynitrite-induced functional impairment of Rat coronary vessels.

Zhijun Sun, Xing Wu, Weiping Li, Hui Peng, Xuhua Shen, Lu Ma, Huirong Liu, Hongwei Li

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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  8. Inhibition of the mevalonate pathway improves myocardial fibrosis.Experimental and therapeutic medicine · 2021
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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

8 authors at 2 institutions in 1 country.

Zhijun SunDepartment of Heart Center, Capital Medical University Affiliated Beijing Friendship Hospital, Beijing, China.
Xing WuDepartment of Heart Center, Capital Medical University Affiliated Beijing Friendship Hospital, Beijing, China.
Weiping LiDepartment of Heart Center, Capital Medical University Affiliated Beijing Friendship Hospital, Beijing, China.
Hui PengDepartment of Heart Center, Capital Medical University Affiliated Beijing Friendship Hospital, Beijing, China.
Xuhua ShenDepartment of Heart Center, Capital Medical University Affiliated Beijing Friendship Hospital, Beijing, China.
Lu MaBeijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, Beijing, People's Republic of China.
Huirong LiuBeijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, Beijing, People's Republic of China.
Hongwei LiDepartment of Heart Center, Capital Medical University Affiliated Beijing Friendship Hospital, Beijing, China. lhw19656@sina.com.
Capital Medical University · CNBeijing Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes-induced vascular dysfunction may arise from reduced nitric oxide (NO) availability, following interaction with superoxide to form peroxynitrite. Peroxynitrite can induce formation of 3-nitrotyrosine-modified proteins. RhoA/ROCK signaling is also involved in diabetes-induced vascular dysfunction. The study aimed to investigate possible links between Rho/ROCK signaling, hyperglycemia, and peroxynitrite in small coronary arteries.

methodsRat small coronary arteries were exposed to normal (NG; 5.5 mM) or high (HG; 23 mM) D-glucose. Vascular ring constriction to 3 mM 4-aminopyridine and dilation to 1 μM forskolin were measured. Protein expression (immunohistochemistry and western blot), mRNA expression (real-time PCR), and protein activity (luminescence-based G-LISA and kinase activity spectroscopy assays) of RhoA, ROCK1, and ROCK2 were determined.

resultsVascular ring constriction and dilation were smaller in the HG group than in the NG group (P < 0.05); inhibition of RhoA or ROCK partially reversed the effects of HG. Peroxynitrite impaired vascular ring constriction/dilation; this was partially reversed by inhibition of RhoA or ROCK. Protein and mRNA expressions of RhoA, ROCK1, and ROCK2 were higher under HG than NG (P < 0.05). This HG-induced upregulation was attenuated by inhibition of RhoA or ROCK (P < 0.05). HG increased RhoA, ROCK1, and ROCK2 activity (P < 0.05). Peroxynitrite also enhanced RhoA, ROCK1, and ROCK2 activity; these actions were partially inhibited by 100 μM urate (peroxynitrite scavenger). Exogenous peroxynitrite had no effect on the expression of the voltage-dependent K

conclusionsPeroxynitrite-induced coronary vascular dysfunction may be mediated, at least in part, through increased expressions and activities of RhoA, ROCK1, and ROCK2.

Indexed as

Gene Expression RegulationAnimalsBlotting, WesternCells, CulturedCoronary Artery DiseaseCoronary VesselsDiabetes Mellitus, ExperimentalDisease Models, AnimalImmunohistochemistryMalePeroxynitrous AcidPhosphorylationRatsRats, Sprague-DawleyReal-Time Polymerase Chain ReactionrhoA GTP-Binding ProteinPeroxynitrous AcidrhoA GTP-Binding Proteinrho-Associated KinasesRNACoronary arteryHyperglycemiaPeroxynitriteRhoA/ROCKVasoconstrictionVasodilation

Identifiers

PMID27724862
PMCPMC5057502
OpenAlexW2530669123

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LicenceCC BY
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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.