High expression of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) associated with Diquat-induced damage.

Ecotoxicol Environ Saf

College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu 211816, China. Electronic address:

Published: August 2024

AI Article Synopsis

  • * Using gene expression data and an animal model of DQ-induced kidney injury, the study identified 21 differentially expressed genes (DEGs) related to stress responses and transcription regulation.
  • * The study highlights HMGCS2 as a key gene linked to DQ-induced damage, suggesting it could serve as a potential diagnostic marker and target for new treatments.

Article Abstract

Diquat (DQ) is a commonly used bipyridine herbicide known for its toxic properties and adverse effects on individuals. However, the mechanism underlying DQ-induced damage remain elusive. Our research aimed to uncover the regulatory network involved in DQ-induced damage. We analyzed publicly accessible gene expression patterns and performed research using a DQ-induced damage animal model. The GSE153959 dataset from the Gene Expression Omnibus collection and the animal model of DQ-induced kidney injury were used to identify differentially expressed genes (DEGs). Pathways including the regulation of DNA-templated transcription in response to stress, RNA polymerase II transcription regulator complex and transcription coregulatory activity were shown to be enriched in 21 DEGs. We used least absolute shrinkage and selection operator (LASSO) regression analysis to find possible diagnostic biomarkers for DQ-induced damage. Then, we used an HK-2 cell model to confirm these results. Additionally, we confirmed that 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) was the major gene associated with DQ-induced damage using multi-omics screening. The sample validation strongly suggested that HMGCS2 has promise as a diagnostic marker and may provide new targets for therapy in the context of DQ-induced damage.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ecoenv.2024.116623DOI Listing

Publication Analysis

Top Keywords

dq-induced damage
24
3-hydroxy-3-methylglutaryl-coa synthase
8
synthase hmgcs2
8
gene expression
8
animal model
8
damage
7
dq-induced
7
high expression
4
expression 3-hydroxy-3-methylglutaryl-coa
4
hmgcs2 associated
4

Similar Publications

[Sulforaphane alleviates acute liver injury induced by diquat in mice by activating Keap1/Nrf2 signaling pathway].

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue

November 2024

Department of Emergency, Kweichow Moutai Hospital, Zunyi 564500, Guizhou, China. Corresponding author: Zhou Manhong, Email:

Objective: To investigate the protective effect and possible mechanism of sulforaphane (SFN) on acute liver injury in mice induced by diquat (DQ) poisoning.

Methods: Forty-eight male C57BL/6 mice were divided into Control group, DQ model group (DQ group), SFN intervention group (DQ+SFN group), and SFN control group (SFN group) using a random number table method, with 12 mice in each group. Acute liver injury mice model was established by one-time intraperitoneal injection of 1 mL of 40 mg/kg DQ solution at once.

View Article and Find Full Text PDF

Diquat exacerbates oxidative stress and neuroinflammation by blocking the autophagic flux of microglia in the hippocampus.

Ecotoxicol Environ Saf

November 2024

Department of Emergency Medicine, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China; Zhejiang Key Laboratory for Diagnosis and Treatment of Physic-chemical and Aging-related Injuries, Hangzhou, Zhejiang 310003, China. Electronic address:

Diquat (DQ) is a widely utilized nonselective herbicide that is primarily used to control a wide range of weeds and crop residues. It also has significant environmental implications. DQ exposure can cause severe damage to the central nervous system (CNS), a critical symptom of acute poisoning that endangers patients.

View Article and Find Full Text PDF

The PI3K/Akt-Nrf2 Signaling Pathway and Mitophagy Synergistically Mediate Hydroxytyrosol to Alleviate Intestinal Oxidative Damage.

Int J Biol Sci

September 2024

State Key Laboratory of Animal Nutrition and Feeding, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing, 100193, China.

Oxidative stress is a major pathogenic factor in many intestinal diseases, such as inflammatory bowel disease (IBD) and colorectal cancer (CRC). The Nrf2 signaling pathway and mitophagy can reduce reactive oxygen species (ROS) and alleviate oxidative stress, but their relationship is unclear. Hydroxytyrosol (HT), a polyphenolic compound abundant in olive oil, has strong antioxidant activity and may help treat these diseases.

View Article and Find Full Text PDF
Article Synopsis
  • Diquat (DQ) poisoning primarily targets the kidneys and leads to multi-organ damage, mainly through increased oxidative stress and inflammation.
  • The study developed red blood cell membrane-camouflaged nanoparticles to deliver Epigallocatechin gallate (EGCG), a compound known for its antioxidant and anti-inflammatory properties, to treat kidney injury caused by DQ.
  • Results showed that the EGCG-RBCm/NPs treatment effectively reduced reactive oxygen species (ROS), apoptosis, and kidney damage markers, indicating its potential as a protective therapy against DQ-induced renal toxicity.
View Article and Find Full Text PDF

High expression of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) associated with Diquat-induced damage.

Ecotoxicol Environ Saf

August 2024

College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu 211816, China. Electronic address:

Article Synopsis
  • * Using gene expression data and an animal model of DQ-induced kidney injury, the study identified 21 differentially expressed genes (DEGs) related to stress responses and transcription regulation.
  • * The study highlights HMGCS2 as a key gene linked to DQ-induced damage, suggesting it could serve as a potential diagnostic marker and target for new treatments.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!