Evidence map›Paper›PMID 41895407›Full record

ReviewBiomedical journal2026

Steatosis paradox: Unraveling pathways of suppressive effect of hepatic steatosis on hepatitis B virus.

Shang-Chin Huang, Jia-Horng Kao

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biomedical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

2 authors.

Shang-Chin HuangDepartment of Internal Medicine, National Taiwan University Hospital Bei-Hu Branch, Taipei, Taiwan; Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan; Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan; Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.
Jia-Horng KaoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan; Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan; Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan. Electronic address: kaojh@ntu.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global intersection of chronic hepatitis B (CHB) and metabolic dysfunction-associated steatotic liver disease (MASLD) has revealed an intriguing clinical paradox: hepatic steatosis is frequently associated with lower hepatitis B virus (HBV) viral loads, higher rates of HBsAg seroclearance, and even favorable clinical outcomes. Accumulating data suggest that lipid accumulation transforms hepatocytes into a hostile microenvironment for HBV through at least four pathways, including immune modulation, metabolic reprogramming, endoplasmic reticulum stress, and impaired autophagy. Deciphering these molecular pathways not only explains the unique natural history of CHB patients with concurrent MASLD but also highlights novel therapeutic targets such as selective modulators of cellular stress that could complement existing antivirals or immune enhancers to facilitate functional cure. In this review, the current evidence regarding the cellular mechanisms underlying the suppressive effect of steatosis on HBV is summarized, providing a translational roadmap for exploiting these virus-host metabolic interactions to develop next-generation, novel host-targeting therapies against HBV.

Indexed as

Fatty LiverHepatitis B, ChronicHepatitis B virusAnimalsAutophagyEndoplasmic Reticulum StressHumansAdiponectinFatty liverFunctional cureHepatic steatosisHepatitis B virus

Identifiers

PMID41895407
PMCPMC13226817

What Socratic holds

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LicenceCC BY
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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.