Evidence map›Paper›PMID 40279007›Full record

ArticleHuman cell2025

Deficiency of synaptotagmin-1 aggravates pressure overload-induced cardiac hypertrophy and dysfunction via the p38 MAPK signaling pathway in mice.

Jing Shen, Junqiu Miao, Lifei Wu, Deping Wang, Guang Li, Haixiong Wang, Jimin Cao

Abstract read
In one paragraph

Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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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

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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

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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.

Jing Shen *Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, Shanxi Medical University, Taiyuan, 030001, China.
Junqiu Miao *Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, Shanxi Medical University, Taiyuan, 030001, China.
Lifei WuKey Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, Shanxi Medical University, Taiyuan, 030001, China.
Deping WangKey Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, Shanxi Medical University, Taiyuan, 030001, China.
Guang LiKey Laboratory of Medical Electrophysiology at Southwest Medical University, Ministry of Education, and the Institute of Cardiovascular Research, Southwest Medical University, Luzhou, 646099, China. liguang@swmu.edu.cn.
Haixiong WangDepartment of Cardiology, Shanxi Cardiovascular Hospital, Taiyuan, 030000, China. cz1976whx@126.com.
Jimin CaoKey Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, Shanxi Medical University, Taiyuan, 030001, China. caojimin@sxmu.edu.cn.

Funding

Applied Basic Research Project of Shanxi Province, China 202103021223239National Natural Science Foundation of China 81670313National Natural Science Foundation of China 82170294National Natural Science Foundation of China 82170523Shanxi "1331" Project Quality and Efficiency Improvement Plan 1331KFC
6 · The paper itself

Abstract

Cardiac hypertrophy is a major risk factor for heart failure and sudden cardiac death, but its molecular mechanisms have not been well clarified. Synaptotagmin-1 (SYT1) is an important regulator of exocytosis and apoptosis and has been found expressed in the myocardium, while its functions in heart diseases have rarely been studied. Here, we investigated the role and mechanism of SYT1 in pressure overload-induced cardiac hypertrophy. Transverse aortic constriction (TAC) surgeries were performed to induce cardiac hypertrophy in global Syt1 knockout (Syt1

Indexed as

CardiomegalyMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesSignal TransductionSynaptotagmin IAngiotensin IIAnimalsApoptosisFibrosisMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumMyocytes, CardiacPhosphorylationAngiotensin IIp38 Mitogen-Activated Protein KinasesSynaptotagmin ISyt1 protein, mouseApoptosisCardiac fibrosisCardiac hypertrophyp38 MAPKSynaptotagmin-1

Identifiers

PMID40279007
PMCPMC12031904

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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.