Evidence map›Paper›PMID 22723782›Full record

ArticleFrontiers in physiology2012

The role of chemokines in acute liver injury.

Yedidya Saiman, Scott L Friedman

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Ethanol reshapes FFC-driven steatohepatitis through time-dependent fibrosis and lipid-droplet remodeling.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  6. Article
  7. Review
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  10. Article
  11. Review
  12. Article
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  14. Pathogenesis, Non-Invasive Assessments and Treatment of Hepatic Fibrosis in Autoimmune Liver Diseases.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  15. Biomarkers as Beacons: Illuminating Sepsis-Associated Hepato-Renal Injury.International journal of molecular sciences · 2025
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

41 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

2 authors at 1 institution in 1 country.

Yedidya SaimanDivision of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine New York, NY, USA.
Scott L Friedman
Icahn School of Medicine at Mount Sinai · US

Funding

MOUNT SINAI MEDICAL SCIENTIST TRAINING PROGRAMT32GM007280 · NIGMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BARON, MARGARET H · 1985 to 2021
$22.8M
The Role of KLF6 in Hepatic FibrosisR01DK056621 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FRIEDMAN, SCOTT L. · 2000 to 2019
$6.2M
Biliary Epithelial Cell-derived SDF-1a in Hepatic Fibrogenesis and InflammationF30DK090986 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SAIMAN, YEDIDYA · 2011 to 2014
$143k
NIDDK NIH HHS F30 DK090986NIDDK NIH HHS R01 DK056621NIGMS NIH HHS T32 GM007280
6 · The paper itself

Abstract

Chemokines are small molecular weight proteins primarily known to drive migration of immune cell populations. In both acute and chronic liver injury, hepatic chemokine expression is induced resulting in inflammatory cell infiltration, angiogenesis, and cell activation and survival. During acute injury, massive parenchymal cell death due to apoptosis and/or necrosis leads to chemokine production by hepatocytes, cholangiocytes, Kupffer cells, hepatic stellate cells, and sinusoidal endothelial cells. The specific chemokine profile expressed during injury is dependent on both the type and course of injury. Hepatotoxicity by acetaminophen for example leads to cellular necrosis and activation of Toll-like receptors while the inciting insult in ischemia reperfusion injury produces reactive oxygen species and subsequent production of pro-inflammatory chemokines. Chemokine expression by these cells generates a chemoattractant gradient promoting infiltration by monocytes/macrophages, NK cells, NKT cells, neutrophils, B cells, and T cells whose activity are highly regulated by the specific chemokine profiles within the liver. Additionally, resident hepatic cells express chemokine receptors both in the normal and injured liver. While the role of these receptors in normal liver has not been well described, during injury, receptor up-regulation, and chemokine engagement leads to cellular survival, proliferation, apoptosis, fibrogenesis, and expression of additional chemokines and growth factors. Hepatic-derived chemokines can therefore function in both paracrine and autocrine fashions further expanding their role in liver disease. More recently it has been appreciated that chemokines can have diverging effects depending on their temporal expression pattern and the type of injury. A better understanding of chemokine/chemokine receptor axes will therefore pave the way for development of novel targeted therapies for the treatment of liver disease.

Indexed as

acute liver injurychemokines

Identifiers

PMID22723782
PMCPMC3379724
OpenAlexW2033260525

What OpenQuestion 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 OpenQuestion graph.