Evidence map›Paper›PMID 35998296›Full record

ArticleJournal of cellular physiology2022

PARP1 inhibition enhances reactive oxygen species on gut microbiota.

Yixiao Zhuang, Hui Wang, Jiyang Ding, Xinyi Zhang, Xiaoyu Liu, Shuai Zhang, Xiaorui Xing, Keneilwe Kenny Kaudimba, Muyang He, Shuang Zhang and 4 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
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

14 authors at 4 institutions in 1 country.

Yixiao ZhuangState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.ORCID 0000-0003-3566-2162
Hui WangShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism & Integrative Biology, Fudan University, Shanghai, China.
Jiyang DingState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Xinyi ZhangState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Xiaoyu LiuCollege of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia, China.
Shuai ZhangCollege of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia, China.
Xiaorui XingSchool of Kinesiology, Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, China.
Keneilwe Kenny KaudimbaSchool of Kinesiology, Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, China.
Muyang HeShanghai Medical College, Fudan University, Shanghai, China.
Shuang ZhangSchool of Kinesiology, Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, China.
Shanshan GuoState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Xingxing KongState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Li JinState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Tiemin LiuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Fudan University · CNShanghai University of Sport · CNInner Mongolia University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase 1 (PARP1) plays a key role in genome stability by modulating DNA-damage responses. Activated by DNA interruptions through ultraviolet (UV) exposure, PARylation is synthesized by PARP1 and serves as a survival mechanism for cancer and metabolic diseases. Several strategies including ROS and antimicrobial peptides (AMPs) function in host defenses, while the targeted tissue and mechanism under DNA damage are unknown. Here, we show that DNA damage induces responses specifically in the gut tissue. The knockdown of PARP1 reduces the activation of PARylation. Parp1 knockdown under DNA damage results in over-accumulated ROS and secretion of AMPs through the regulation of Relish, a subunit of nuclear factor-κB (NF-κB). Double-knockdown of Parp1 and Relish specifically in the gut inhibits AMP secretion. In conclusion, the host defense is achieved through ROS accumulation rather than the AMPs under DNA damage. In contrast, the knockdown of PARP1 exacerbates ROS accumulation to a harmful level. Under this circumstance, NF-κb targeted AMP secretion is provoked for host defense. Microbiome and functional analysis provide evidence for the hazard of DNA damage and show variations in the metabolic pathways following Parp1 inhibition. Our findings suggest the notion that PARP1 inhibition contributes to ROS accumulation under DNA damage and its role in NF-κb activation for host defense.

Indexed as

Gastrointestinal MicrobiomeNF-kappa BDNADNA DamagePoly (ADP-Ribose) Polymerase-1Reactive Oxygen SpeciesDNANF-kappa BPoly (ADP-Ribose) Polymerase-1Reactive Oxygen Speciesgut microbiotaNF-κBpoly(ADP-ribose) polymerase 1ROSUV

Identifiers

PMID35998296
PMCPMC9805012
OpenAlexW4292982626

What OpenQuestion 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 OpenQuestion graph.