Evidence map›Paper›PMID 35260820›Full record

ArticleActa pharmacologica Sinica2022

Chronic infusion of ELABELA alleviates vascular remodeling in spontaneously hypertensive rats via anti-inflammatory, anti-oxidative and anti-proliferative effects.

Chao Ye, Zhi Geng, Ling-Li Zhang, Fen Zheng, Ye-Bo Zhou, Guo-Qing Zhu, Xiao-Qing Xiong

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  14. Wogonin attenuates vascular remodeling by inhibiting smooth muscle cell proliferation and migration in hypertensive rat.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
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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

7 authors at 2 institutions in 1 country.

Chao Ye *Key Laboratory of Targeted Intervention of Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Zhi Geng *Department of Cardiac Surgery, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 211166, China.
Ling-Li ZhangDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 211166, China.
Fen ZhengKey Laboratory of Targeted Intervention of Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Ye-Bo ZhouKey Laboratory of Targeted Intervention of Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Guo-Qing ZhuKey Laboratory of Targeted Intervention of Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Xiao-Qing XiongKey Laboratory of Targeted Intervention of Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing, 211166, China. xqxiong@njmu.edu.cn.
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory activation and oxidative stress promote the proliferation of vascular smooth muscle cells (VSMCs), which accounts for pathological vascular remodeling in hypertension. ELABELA (ELA) is the second endogenous ligand for angiotensin receptor-like 1 (APJ) receptor that has been discovered thus far. In this study, we investigated whether ELA regulated VSMC proliferation and vascular remodeling in spontaneously hypertensive rats (SHRs). We showed that compared to that in Wistar-Kyoto rats (WKYs), ELA expression was markedly decreased in the VSMCs of SHRs. Exogenous ELA-21 significantly inhibited inflammatory cytokines and NADPH oxidase 1 expression, reactive oxygen species production and VSMC proliferation and increased the nuclear translocation of nuclear factor erythroid 2-related factor (Nrf2) in VSMCs. Osmotic minipump infusion of exogenous ELA-21 in SHRs for 4 weeks significantly decreased diastolic blood pressure, alleviated vascular remodeling and ameliorated vascular inflammation and oxidative stress in SHRs. In VSMCs of WKY, angiotensin II (Ang II)-induced inflammatory activation, oxidative stress and VSMC proliferation were attenuated by pretreatment with exogenous ELA-21 but were exacerbated by ELA knockdown. Moreover, ELA-21 inhibited the expression of matrix metalloproteinase 2 and 9 in both SHR-VSMCs and Ang II-treated WKY-VSMCs. We further revealed that exogenous ELA-21-induced inhibition of proliferation and PI3K/Akt signaling were amplified by the PI3K/Akt inhibitor LY294002, while the APJ receptor antagonist F13A abolished ELA-21-induced PI3K/Akt inhibition and Nrf2 activation in VSMCs. In conclusion, we demonstrate that ELA-21 alleviates vascular remodeling through anti-inflammatory, anti-oxidative and anti-proliferative effects in SHRs, indicating that ELA-21 may be a therapeutic agent for treating hypertension.

Indexed as

HypertensionPeptide HormonesVascular RemodelingAngiotensin IIAnimalsAnti-Inflammatory AgentsCells, CulturedCytokinesLigandsMatrix Metalloproteinase 2Muscle, Smooth, VascularNADPH Oxidase 1NF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsAngiotensin IIAnti-Inflammatory AgentsCytokinesLigandsMatrix Metalloproteinase 2NADPH Oxidase 1NF-E2-Related Factor 2Peptide HormonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptors, AngiotensinELABELA peptidehypertensioninflammationoxidative stressproliferationvascular remodeling

Identifiers

PMID35260820
PMCPMC9525578
OpenAlexW4220723214

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.