Evidence map›Paper›PMID 33184797›Full record

ArticleDigestive diseases and sciences2021

DNA Damage-Regulated Autophagy Modulator 1 (DRAM1) Mediates Autophagy and Apoptosis of Intestinal Epithelial Cells in Inflammatory Bowel Disease.

Yu Zhang, Xiaozhi Li, Yaoting Li, Ying Li, Ying Wang, Liguo Zhu, Peng Chen, Zhenyi Tian, Yun Qiu, Rui Feng and 6 more

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 1 country.

Yu Zhang *Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Xiaozhi Li *Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Yaoting Li *Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Ying LiDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Ying WangDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Liguo ZhuDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Peng ChenDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Zhenyi TianDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Yun QiuDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Rui FengDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Zhirong ZengDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Yao HeDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Baili ChenDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Shenghong ZhangDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Ren Mao *Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China.
Minhu Chen *Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China. chenminhu@mail.sysu.edu.cn.
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsDNA damage-regulated autophagy modulator 1 (DRAM1) is required for induction of autophagy and apoptosis. However, the influence of DRAM1 on the pathogenesis of inflammatory bowel disease (IBD) has not been explored.

methodsDRAM1 expression was examined in the intestinal mucosa of patients with IBD and colons of colitis mice. We used a recombinant adeno-associated virus carrying small hairpain DRAM1 to knock down the DRAM1 gene to treat colitis in the mice. The effect of DRAM1 on autophagy and apoptosis of intestinal epithelial cells was explored. DRAM1-mediated interaction with the c-Jun N-terminal kinase (JNK) pathway was also examined.

resultsDRAM1 expression in the intestinal mucosa of the IBD patients was higher than that in the control participates. DRAM1 expression in the inflammatory cells in patients with Crohn's disease (CD) was lower than that in patients with ulcerative colitis (UC). Additionally, DRAM1 expression was correlated with the Simple Endoscopic Score for CD and the Mayo endoscopic score for UC. Serum levels of DRAM1 in the IBD group were substantially higher than those in the normal group. The knockdown of DRAM1 could alleviate colitis symptoms in mice. In in vitro experiments, knocking down DRAM1 could reduce autophagy and apoptosis levels. Mechanistically, DRAM1 may participate in the regulation of these two processes by positively regulating JNK activation.

conclusionsDuring intestinal inflammation, the upregulation of DRAM1 may promote the activation of JNK and further aggravate intestinal epithelium damage.

Indexed as

AdolescentAdultAgedAnimalsApoptosisAutophagyChildColitisDextran SulfateEpithelial CellsFemaleHumansInflammatory Bowel DiseasesIntestinal MucosaMaleMembrane ProteinsDextran SulfateDRAM1 protein, humanDRAM-1 protein, mouseMembrane ProteinsTrinitrobenzenesulfonic AcidApoptosisAutophagyDRAM1Inflammatory bowel diseaseIntestinal inflammationJNK

Identifiers

PMID33184797
OpenAlexW3098207024

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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.