Evidence map›Paper›PMID 37202387›Full record

ArticleCell death & disease2023

Butyrate limits inflammatory macrophage niche in NASH.

Ankita Sarkar, Priya Mitra, Abhishake Lahiri, Tanusree Das, Jit Sarkar, Sandip Paul, Partha Chakrabarti

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
18.2field-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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Short-chain fatty acids.Nature metabolism · 2026
    Review
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  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
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  13. Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

6 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

7 authors at 1 institution in 1 country.

Ankita SarkarDivision of Cell Biology and Physiology, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Priya MitraDivision of Cell Biology and Physiology, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Abhishake LahiriDivision of Structural Biology & Bioinformatics, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Tanusree DasDivision of Cell Biology and Physiology, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Jit SarkarElucidata, New Delhi, Delhi, 110017, India.
Sandip PaulJIS Institute of Advanced Studies & Research, Kolkata, India.ORCID 0000-0001-7406-3598
Partha ChakrabartiDivision of Cell Biology and Physiology, CSIR-Indian Institute of Chemical Biology, Kolkata, India. pchakrabarti@iicb.res.in.ORCID 0000-0001-9502-8695
Indian Institute of Chemical Biology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune cell infiltrations with lobular inflammation in the background of steatosis and deregulated gut-liver axis are the cardinal features of non-alcoholic steatohepatitis (NASH). An array of gut microbiota-derived metabolites including short-chain fatty acids (SCFA) multifariously modulates NASH pathogenesis. However, the molecular basis for the favorable impact of sodium butyrate (NaBu), a gut microbiota-derived SCFA, on the immunometabolic homeostasis in NASH remains elusive. We show that NaBu imparts a robust anti-inflammatory effect in lipopolysaccharide (LPS) stimulated or classically activated M1 polarized macrophages and in the diet-induced murine NASH model. Moreover, it impedes monocyte-derived inflammatory macrophage recruitment in liver parenchyma and induces apoptosis of proinflammatory liver macrophages (LM) in NASH livers. Mechanistically, by histone deactylase (HDAC) inhibition NaBu enhanced acetylation of canonical NF-κB subunit p65 along with its differential recruitment to the proinflammatory gene promoters independent of its nuclear translocation. NaBu-treated macrophages thus exhibit transcriptomic signatures that corroborate with a M2-like prohealing phenotype. NaBu quelled LPS-mediated catabolism and phagocytosis of macrophages, exhibited a differential secretome which consequently resulted in skewing toward prohealing phenotype and induced death of proinflammatory macrophages to abrogate metaflammation in vitro and in vivo. Thus NaBu could be a potential therapeutic as well as preventive agent in mitigating NASH.

Indexed as

Non-alcoholic Fatty Liver DiseaseAnimalsButyric AcidLipopolysaccharidesLiverMacrophagesMiceMice, Inbred C57BLButyric AcidLipopolysaccharides

Identifiers

PMID37202387
PMCPMC10195803
OpenAlexW4377047450

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.