Evidence mapPaperPMID 42544644Full record

ArticleAging cell2026

Endothelial AGGF1 Deficiency Causes Mitochondrial Dysfunction and Contributes to Age-Elevated Blood Pressure.

Weixin Lv, Xiaojuan Zhong, Qiang Yuan, Xueting Gong, Ya Zhao, Shilin Zhang, Andong Wu, Ming Wan, Xueer Li, Yangyi Zheng and 7 more

Abstract read
In one paragraph

Article in Aging cell, 2026. 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
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
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

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

17 authors.

Weixin LvAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Xiaojuan ZhongAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Qiang YuanAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Xueting GongAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.ORCID https://orcid.org/0000-0002-1197-3452
Ya ZhaoAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.ORCID https://orcid.org/0009-0008-6971-0402
Shilin ZhangAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Andong WuAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Ming WanAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Xueer LiAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.ORCID https://orcid.org/0009-0005-8882-6169
Yangyi ZhengAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Jiankun LiuAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Bingbing ZhouAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Yuanzheng ZhuAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Limin ZhaoHuman Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.
Qiquan WangMetabolic Control and Aging, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.ORCID https://orcid.org/0000-0001-5265-1065
Yang XiangMetabolic Control and Aging, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.ORCID https://orcid.org/0000-0003-3016-0323
Xiao-Li TianAging and Vascular Diseases, Human Aging Research Institute (HARI) and School of Life Science, Nanchang University, and Jiangxi Province Key Laboratory of Aging and Disease, Nanchang, Jiangxi, China.ORCID https://orcid.org/0000-0002-0868-7025

Funding

Jiangxi Province Key Laboratory of Aging and Disease 2024SSY07161National Key Research and Development Program of the Ministry of Science and Technology, China 2023YFC3603300National Natural Science Foundation of China 82330046
6 · The paper itself

Abstract

Endothelial cells are critical in the regulation of blood pressure. We previously demonstrated AGGF1 was crucial for maintaining endothelial cell function. This study aims to examine whether AGGF1 regulates blood pressure. Here, we found that AGGF1 expression was inversely correlated with blood pressure with age. In male mice, endothelial-specific loss of function of Aggf1 (Aggf1

Indexed as

AgingAngiogenic ProteinsBlood PressureEndothelial CellsMitochondriaAnimalsHumansMaleMiceMice, Inbred C57BLNitric Oxide Synthase Type IIIReactive Oxygen SpeciesAGGF1 protein, humanAggf1 protein, mouseAngiogenic ProteinsNitric Oxide Synthase Type IIIReactive Oxygen SpeciesAGGF1blood pressureearly vascular agingendothelial cellmitochondrial dysfunctionSESN2

Identifiers

PMID42544644
PMCPMC13430426

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.