Evidence map›Paper›PMID 34601668›Full record

ArticleMolecular neurobiology2021

Sigma-1 Receptor Activation Suppresses Microglia M1 Polarization via Regulating Endoplasmic Reticulum-Mitochondria Contact and Mitochondrial Functions in Stress-Induced Hypertension Rats.

Kokwin Ooi, Li Hu, Yi Feng, Chenzhi Han, Xiaorong Ren, Xinyi Qian, Haofeng Huang, Sijia Chen, Qi Shi, Hong Lin and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 60 citations in OpenAlex.

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  17. Electrical Stimulation Therapy - Dedicated to the Perfect Plastic Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

14 authors at 4 institutions in 1 country.

Kokwin OoiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Li HuDepartment of Cardiovascular Diseases, Renji Hospital Affiliated To Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Yi FengDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, People's Republic of China.
Chenzhi HanDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Xiaorong RenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Xinyi QianDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Haofeng HuangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Sijia ChenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Qi ShiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Hong LinDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Jijiang WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Danian ZhuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China.
Rui WangDepartment of Cardiovascular Diseases, Yangpu District Central Hospital Affiliated to Tongji University School of Medicine, Shanghai, 200090, People's Republic of China. wangruino1@sina.com.
Chunmei XiaDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China. cmxia@fudan.edu.cn.ORCID http://orcid.org/0000-0001-9845-9685
Fudan University · CNShanghai Jiao Tong University · CNShanghai Medical College of Fudan University · CNYangpu Hospital of Tongji University · CN

Funding

National Natural Science Foundation of China 31271215National Natural Science Foundation of China 81770423
6 · The paper itself

Abstract

Exposure to stress plays a detrimental role in the pathogenesis of hypertension via neuroinflammation pathways. Microglial neuroinflammation in the rostral ventrolateral medulla (RVLM) exacerbates stress-induced hypertension (SIH) by increasing sympathetic hyperactivity. Mitochondria of microglia are the regulators of innate immune response. Sigma-1R (σ-1R) localizes to the mitochondria-associated membranes (MAMs) and regulates endoplasmic reticulum (ER) and mitochondria communication, in part through its chaperone activity. The present study aims to investigate the protective role of σ-1R on microglial-mediated neuroinflammation. Stress-induced hypertension (SIH) was induced in rats using electric foot shocks and intermittent noise. Arterial blood pressure (ABP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were measured to evaluate the sympathetic nervous system (SNS) activities. SKF10047 (100 µM), an agonist of σ-1R, was administrated to rats, then σ-1R localization and MAM alterations were detected by immuno-electron microscopy. Mitochondrial calcium homeostasis was examined in primary microglia and/or BV-2 microglia cells. The effect of SKF10047 treatment on the mitochondrial respiratory function of cultured microglia was measured using a Seahorse Extracellular Flux Analyzer. Confocal microscopic images were performed to indicate mitochondrial dynamics. Stress reduces σ-1R's localization at the MAMs, leading to decreased ER-mitochondria contact and IP3R-GRP75-VDAC calcium transport complexes expression in the RVLM of rats. SKF10047 promotes the length and coverage of MAMs in the prorenin-treated microglia. Prorenin treatment increases mitoROS levels, and inhibits Ca

Indexed as

AnimalsBlood PressureCalciumCell PolarityElectroshockEndoplasmic ReticulumHeart RateHypertensionMicrogliaMitochondriaPhenazocineRatsReceptors, sigmaSigma-1 ReceptorSympathetic Nervous SystemCalciumPhenazocineReceptors, sigmaSigma-1 ReceptorSK&F 10047HypertensionNeuroinflammationSigma-1 receptorStressSympathetic nervous system

Identifiers

PMID34601668
OpenAlexW3127173425

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.