Evidence map›Paper›PMID 34269955›Full record

ArticleCardiovascular toxicology2021

Inhibition of Maternal c-Src Ameliorates the Male Offspring Hypertension by Suppressing Inflammation and Neurotransmitters in the Paraventricular Nucleus.

Qing Su, Xiao-Jing Yu, Qing Yang, Xiao-Min Wang, Wen-Jie Xia, Hong-Bao Li, Kai-Li Liu, Qiu-Yue Yi, Yu-Ming Kang

Abstract read
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In one paragraph

Article in Cardiovascular toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
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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

9 authors at 3 institutions in 1 country.

Qing Su *Department of Physiology and Pathophysiology, Shaanxi Engineering and Research Center of Vaccine, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry of China, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, 710061, China.
Xiao-Jing Yu *Department of Physiology and Pathophysiology, Shaanxi Engineering and Research Center of Vaccine, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry of China, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, 710061, China. xiaojingyu621@163.com.
Qing YangSchool of Sport and Health Sciences, Xi'an Physical Education University, Xi'an, 710068, China.
Xiao-Min WangDepartment of Physiology and Pathophysiology, Shaanxi Engineering and Research Center of Vaccine, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry of China, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, 710061, China.
Wen-Jie XiaDepartment of Physiology and Pathophysiology, Shaanxi Engineering and Research Center of Vaccine, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry of China, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, 710061, China.
Hong-Bao LiDepartment of Physiology and Pathophysiology, Shaanxi Engineering and Research Center of Vaccine, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry of China, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, 710061, China.
Kai-Li LiuDepartment of Physiology and Pathophysiology, Shaanxi Engineering and Research Center of Vaccine, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry of China, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, 710061, China.
Qiu-Yue YiClinical Pharmacological Institution, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.
Yu-Ming KangDepartment of Physiology and Pathophysiology, Shaanxi Engineering and Research Center of Vaccine, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry of China, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, 710061, China. ykang@mail.xjtu.edu.cn.
Xi'an Jiaotong University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Physical Education University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term maternal salt intake induces the hypertension in offspring. Numerous studies have also indicated that high-salt diet causes the inflammation and an imbalance in neurotransmitters in the paraventricular nucleus (PVN) which increases the blood pressure and sympathetic activity. This study aimed to explore whether maternal salt intake induces hypertension in their male offspring by increasing the inflammation and changing the neurotransmitters balance in the paraventricular nucleus of offspring. This study includes two parts: Part I to explore the effect of high-salt diet on pregnant rats and the changes in inflammation and neurotransmitters in their male offspring PVN; Part II to reveal the influence on their offspring of bilateral PVN infusion of c-Src inhibitor dasatinib (DAS) in pregnant rats fed a high-salt diet. Maternal high-salt diet intake during copulation, pregnancy, and lactation impacted the offspring mean arterial pressure (MAP) and elevated the offspring PVN levels of p-Src, proinflammatory cytokines, and excitatory neurotransmitters. Bilateral PVN infusion of a c-Src inhibitor combined with maternal high-salt diets decreased MAP in the offspring. The infusion was also shown to suppress the Src-induced MAPK/NF-κB signaling pathway (p38 MAPK, JNK, Erk1/2), which attenuates inflammatory reactions. Finally, bilateral PVN infusion of the Src inhibitor in pregnant rat with high-salt diets improved the levels of inhibitory neurotransmitters in offspring PVN, which restored the excitatory-inhibitory neurotransmitter balance in male offspring. High-salt diets increase sympathetic activity and blood pressure in adult offspring, probably by activating the c-Src/MAPKs/NF-κB signaling pathway-induced inflammation. Moreover, NF-κB disrupts the downstream excitatory-inhibitory neurotransmitter balance in the PVN of male offspring.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsAntihypertensive AgentsArterial PressureDasatinibDisease Models, AnimalFemaleHypertensionInflammation MediatorsMaleMaternal ExposureMitogen-Activated Protein KinasesNeurotransmitter AgentsNF-kappa BParaventricular Hypothalamic NucleusPregnancyAntihypertensive AgentsDasatinibInflammation MediatorsMitogen-Activated Protein KinasesNeurotransmitter AgentsNF-kappa BProtein Kinase InhibitorsSodium Chloride, Dietarysrc-Family Kinasesc-SrcInflammationMaternal high-salt dietsNeurotransmittersOffspring

Identifiers

PMID34269955
OpenAlexW3179018405

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.