Evidence map›Paper›PMID 39447891›Full record

ArticleThe Science of the total environment2024

Kidney toxicology of a novel compound Lithium Bis(trifluoromethanesulfonyl)imide (LiTFSI, ie. HQ-115) used in energy applications: An epigenetic perspective.

Mia Sands, Xing Zhang, Joseph Irudayaraj

Abstract read
In one paragraph

Article in The Science of the total environment, 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. Article
  3. A CpG Epigenetic Switch Reverts PFAS ToxicityAn In Vitro Study.Environment & health (Washington, D.C.) · 2025
    Article
  4. 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

3 authors.

Mia SandsDepartment of Bioengineering, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA; Carl Woese Institute for Genomic Biology, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA; Biomedical Research Center, Mills Breast Cancer Institute, Carle Foundation Hospital, Urbana, IL 61801, USA.
Xing ZhangDepartment of Bioengineering, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA.
Joseph IrudayarajDepartment of Bioengineering, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA; Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois Urbana-Champaign, Urbana, IL 61801, USA; Carl Woese Institute for Genomic Biology, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA; Cancer Center at Illinois, Beckman Institute, Carle-Illinois College of Medicine, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA; Biomedical Research Center, Mills Breast Cancer Institute, Carle Foundation Hospital, Urbana, IL 61801, USA. Electronic address: jirudaya@illinois.edu.

Funding

Research Training Program in Toxicology and Environmental HealthT32ES007326 · NIEHS · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI Jodi A. Flaws · 2000 to 2026
$8.7M
NIEHS NIH HHS T32 ES007326
6 · The paper itself

Abstract

Exposure to emerging energy-based environmental contaminants such as lithium bis(trifluoromethanesulfonyl)imide (LiTFSI, trade name HQ-115), poses a significant threat to human health, yet its impact on kidney function and epigenetic regulation remains poorly understood. Here, we investigated the effects of LiTFSI exposure on kidney-related biochemical indicators, renal injuries, and epigenetic alterations in male CD-1 mice under both 14-day and 30-day exposure durations. Our study revealed that LiTFSI exposure led to changes in kidney-related markers, notably affecting serum bicarbonate levels, while relative kidney weight remained unaffected. Histological analysis revealed tubule dilation, inflammation, and loss of kidney structure in LiTFSI-exposed mice, alongside dysregulated expression of genes associated with inflammation, renal function, and uric acid metabolism. Epigenetic analysis further identified widespread DNA methylation changes in the two exposure regimes. Functional analysis revealed that differentially methylated regions are implicated in cell apoptosis and cancer-related pathways and are enriched with development-related transcription factor binding motifs, suggesting a potential mechanism of action underlying exposure induced kidney damage. These findings underscore the intricate interplay between environmental exposures, epigenetic modulation, and kidney health, emphasizing the need for additional research to unravel precise mechanisms and develop targeted interventions to mitigate the adverse effects of LiTFSI and exposure of similar clean energy compounds on human health.

Indexed as

Epigenesis, GeneticKidneyAnimalsDNA MethylationEnvironmental PollutantsImidesMaleMiceEnvironmental PollutantsImidesDNA methylationLithium Bis(trifluoromethanesulfonyl)imide (LiTFSI, ie. HQ-115)NephrotoxicityPFASPFOAUric acid metabolism

Identifiers

PMID39447891
PMCPMC12186188

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.