Evidence map›Paper›PMID 39935443›Full record

ArticleJournal of geriatric cardiology : JGC2024

The effects of hypothalamic microglial activation on ventricular arrhythmias in stress cardiomyopathy.

Peng-Qi Lin, Quan-Wei Pei, Bin Li, Jie-Mei Yang, Li-Na Zou, De-Zhan Su, Jun-Pei Zhang, Hong-Peng Yin, Mbabazi Nadine, Jun-Jie Yang and 5 more

Abstract read
In one paragraph

Article in Journal of geriatric cardiology : JGC, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Peng-Qi LinDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Quan-Wei PeiDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Bin LiDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jie-Mei YangDepartment of Echocardiography, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Li-Na ZouDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
De-Zhan SuDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jun-Pei ZhangDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Hong-Peng YinDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Mbabazi NadineDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jun-Jie YangDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Nevzorova Vera AInstitute Therapy and Instrumental Diagnostic, Pacific State Medical University, Vladivostok, Russia.
Khan Musawir AbbasDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhao-Lei JiangDepartment of Cardiothoracic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Jing-Jie LiDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
De-Chun YinDepartment of Geriatrics, the First Affiliated Hospital of Harbin Medical University, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Stress cardiomyopathy (SCM) currently has a high incidence in older adults, and the theories regarding its causes include "catecholamine myocardial toxicity" and "sympathetic hyperactivation". However, the role of the central nervous system in the pathogenesis of SCM remains unknown. We investigated the role of microglia activation in the paraventricular hypothalamic nucleus (PVN) in the development of SCM. Methods: An SCM model was created using male Sprague-Dawley (SD) rats, immobilized for 6 h every day for a week. Electrocardiogram, cardiac electrophysiology, and echocardiography examinations were performed to verify the changes in cardiac structure and function in rats with SCM. RNA sequencing was used to explore the changes in the hypothalamus during SCM. In addition, brain and heart tissues were collected to detect microglial activation and sympathetic activity. Results: The main findings were as follows: (1) immobilization stress successfully induced SCM in SD rats; (2) microglia were significantly activated in the hypothalamus, as evidenced by cytosol thickening, increases in the number of microglial branches, and microglia enriched in the PVN; (3) in SCM, the microglia in the PVN exhibited increased central and peripheral cardiac sympathetic activity and increased the expression of neuroinflammatory factors; and (4) it is possible that inhibiting microglial activation could suppress the sympathetic activity of the central nervous system and heart and increase cardiac electrical stability in SCM rats. Conclusions: SCM was induced in SD rats by immobilization stress, acting through the activation of the hypothalamic microglia. The activated microglia were specifically enriched in the PVN, increasing the activity of the central and peripheral sympathetic nervous systems by regulating the expression of neuro-inflammatory factors, mediating dysfunction of the left ventricle, and increasing the susceptibility to ventricular arrhythmias.

Identifiers

PMID39935443
PMCPMC11808488

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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.