Evidence map›Paper›PMID 39147926›Full record

ArticleCell biology and toxicology2024

Cocaine-derived hippuric acid activates mtDNA-STING signaling in alcoholic liver disease: Implications for alcohol and cocaine co-abuse.

Hwan Ma, Gyu-Rim Lee, Jeong-Su Park, Jin Lee, Feng Wang, Yuanqiang Ma, Guo-Yan Sui, Nodir Rustamov, Sou Hyun Kim, Young-Suk Jung and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell biology and toxicology, 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. Article
  2. Article
  3. Article
  4. 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

15 authors.

Hwan MaCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Gyu-Rim LeeCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Jeong-Su ParkCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Jin LeeDepartment of Pathology, School of Medicine, University of California, San Diego, La Jolla, CA, 92093, USA.
Feng WangCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Yuanqiang MaCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Guo-Yan SuiCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Nodir RustamovCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Sou Hyun KimDepartment of Pharmacy, College of Pharmacy, Pusan National University, Busan, 46241, South Korea.
Young-Suk JungDepartment of Pharmacy, College of Pharmacy, Pusan National University, Busan, 46241, South Korea.
Hwan-Soo YooCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Sang-Bae HanCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Jin Tae HongCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea.
Jaesuk YunCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea. jyun@cbnu.ac.kr.
Yoon Seok RohCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, 28160, South Korea. ysroh@cbnu.ac.kr.

Funding

Korean Food and Drug Administration 20182MFDS425National Research Foundation of Korea 2017R1A5A2015541Regional Innovation Strategy (RIS) of National Research Foundation of Korea 2021RIS-001
6 · The paper itself

Abstract

The simultaneous abuse of alcohol-cocaine is known to cause stronger and more unpredictable cellular damage in the liver, heart, and brain. However, the mechanistic crosstalk between cocaine and alcohol in liver injury remains unclear. The findings revealed cocaine-induced liver injury and inflammation in both marmosets and mice. Of note, co-administration of cocaine and ethanol in mice causes more severe liver damage than individual treatment. The metabolomic analysis confirmed that hippuric acid (HA) is the most abundant metabolite in marmoset serum after cocaine consumption and that is formed in primary marmoset hepatocytes. HA, a metabolite of cocaine, increases mitochondrial DNA leakage and subsequently increases the production of proinflammatory factors via STING signaling in Kupffer cells (KCs). In addition, conditioned media of cocaine-treated KC induced hepatocellular necrosis via alcohol-induced TNFR1. Finally, disruption of STING signaling in vivo ameliorated co-administration of alcohol- and cocaine-induced liver damage and inflammation. These findings postulate intervention of HA-STING-TNFR1 axis as a novel strategy for treatment of alcohol- and cocaine-induced excessive liver damage.

Indexed as

CocaineDNA, MitochondrialHippuratesLiver Diseases, AlcoholicMembrane ProteinsSignal TransductionAnimalsCocaine-Related DisordersEthanolHepatocytesKupffer CellsLiverMaleMiceMice, Inbred C57BLReceptors, Tumor Necrosis Factor, Type ICocaineDNA, MitochondrialEthanolHippurateshippuric acidMembrane ProteinsReceptors, Tumor Necrosis Factor, Type ISting1 protein, mouseSTING ProteinCocaineHippuric acidLiver diseaseMitochondrial DNA leakageSTINGTNFR1

Identifiers

PMID39147926
PMCPMC11327214

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.