Evidence map›Paper›PMID 28486401›Full record

ReviewInternational journal of molecular sciences2017

Drug-Induced Liver Injury: Cascade of Events Leading to Cell Death, Apoptosis or Necrosis.

Andrea Iorga, Lily Dara, Neil Kaplowitz

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
27.7field-weighted citation impact, top 1% 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

139 citing papers in PubMed, 288 citations in OpenAlex.

  1. Article
  2. Systematic comparison of temporal hepatotoxicant-induced gene network responses across 3 liver test systems.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  3. Article
  4. Review
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  9. Review
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  12. AIVIVE: a novel AI framework for enhanced in vitro to in vivo extrapolation (IVIVE) of toxicogenomics data.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Mechanisms of drug induced liver injury.Cellular and molecular life sciences : CMLS · 2025
    Review
  20. Article

79 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Andrea IorgaResearch Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. iorga@usc.edu.
Lily DaraResearch Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. dara@usc.edu.
Neil KaplowitzResearch Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. kaplowit@usc.edu.
University of Southern California · US

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KANEL, GARY · 1995 to 2020
$21.8M
Role of Glutathione Redox Status in HepatotoxicityR01DK067215 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 2005 to 2019
$5.6M
Role of RIPK1 and RIPK3 in liver injury.K08DK109141 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DARA, LILY · 2016 to 2021
$925k
NIDDK NIH HHS K08 DK109141NIDDK NIH HHS P30 DK048522NIDDK NIH HHS R01 DK067215
6 · The paper itself

Abstract

Drug-induced liver injury (DILI) can broadly be divided into predictable and dose dependent such as acetaminophen (APAP) and unpredictable or idiosyncratic DILI (IDILI). Liver injury from drug hepatotoxicity (whether idiosyncratic or predictable) results in hepatocyte cell death and inflammation. The cascade of events leading to DILI and the cell death subroutine (apoptosis or necrosis) of the cell depend largely on the culprit drug. Direct toxins to hepatocytes likely induce oxidative organelle stress (such as endoplasmic reticulum (ER) and mitochondrial stress) leading to necrosis or apoptosis, while cell death in idiosyncratic DILI (IDILI) is usually the result of engagement of the innate and adaptive immune system (likely apoptotic), involving death receptors (DR). Here, we review the hepatocyte cell death pathways both in direct hepatotoxicity such as in APAP DILI as well as in IDILI. We examine the known signaling pathways in APAP toxicity, a model of necrotic liver cell death. We also explore what is known about the genetic basis of IDILI and the molecular pathways leading to immune activation and how these events can trigger hepatotoxicity and cell death.

Indexed as

ApoptosisAnimalsChemical and Drug Induced Liver InjuryHepatocytesHumansNecrosisToxicity TestsacetaminophenadaptationapoptosisDILIhepatotoxicityhuman leukocyte antigen (HLA)necrosis

Identifiers

PMID28486401
PMCPMC5454931
OpenAlexW2613326943

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.