Evidence map›Paper›PMID 39730568›Full record

ArticleScientific reports2024

[Gly14]-Humanin ameliorates high glucose-induced endothelial senescence via SIRT6.

Muqin Li, Zhihua Liu, Xueqin Cao, Wenjin Xiao, Shurong Wang, Chengyuan Zhao, Ying Zhao, Ying Xie

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. The Role of Cellular Senescence in Oral Health and Disease.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025
    Review
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

8 authors.

Muqin Li *Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Zhihua Liu *Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Xueqin Cao *Department of Endocrinology, The Fourth Affiliated Hospital of Soochow University, Chongwen Road No. 9, Suzhou, 215000, Jiangsu, China.
Wenjin XiaoDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Shurong WangDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Chengyuan ZhaoDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Ying ZhaoDepartment of Pathology and Pathophysiology, School of Basic Medical Sciences, Soochow Medical College of Soochow University, Suzhou, 215123, China. yzhao@suda.edu.cn.
Ying XieDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China. 13013883877@126.com.

Funding

Conversion Base - Endocrinology and Metabolism ML12301323National Natural Science Foundation of China 81670742Suzhou Municipal Health Commission SKJY2021082
6 · The paper itself

Abstract

High glucose (HG) induced endothelial senescence is related to endothelial dysfunction and cardiovascular complications in diabetic patients. Humanin, a member of mitochondrial derived peptides (MDPs), is thought to contribute to aging-related cardiovascular protection. The goal of the study is to explore the pathogenesis of HG-induced endothelial senescence and potential anti-senescent effects of Humanin. Human umbilical vein endothelial cells (HUVECs) were exposed to glucose to induce senescence, determined by β-galactosidase staining and the expressions of p21, p53, and p16. A clinically relevant dose of HG (15 mM, HG) induced endothelial senescence after 72 h incubation without elevated apoptosis. HG-induced senescence was attributed to the induction of reactive oxygen species (ROS) caused by SIRT6 downregulation, as ROS inhibitor N-acetyl cysteine blocked HG-induced senescence, while inactivation of SIRT6 increased ROS levels and promoted senescence. Strikingly. pretreatment with [Gly14]-Humanin (HNG) antagonized the downregulation of SIRT6 in response to HG and alleviated ROS production and cell senescence. HG-induced reduction of SIRT6 results in ROS overproduction and endothelial senescence. Humanin protects against HG-induced endothelial senescence via SIRT6. This study provides new directions for biological products related to Humanin to be a potential candidate for the prevention of vascular aging in diabetes.

Indexed as

Cellular SenescenceGlucoseHuman Umbilical Vein Endothelial CellsReactive Oxygen SpeciesSirtuinsHumansIntracellular Signaling Peptides and ProteinsGlucosehumaninIntracellular Signaling Peptides and ProteinsReactive Oxygen SpeciesSIRT6 protein, humanSirtuinsEndothelial cellsHumaninReactive oxygen speciesSenescenceSIRT6

Identifiers

PMID39730568
PMCPMC11681169

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.