# Recent trends in lipid metabolism research in liver cancer: a bibliometric analysis

**Authors:** Yaru Shi, Xinyu Yang, Yunfeng Yu, Yanan Bai, Pei Liu, Jianzhong Cao, Weibin Xie

PMC · DOI: 10.3389/fonc.2026.1704007 · 2026-03-19

## TL;DR

This study maps recent trends in lipid metabolism research in liver cancer, highlighting key areas and future directions from 2014 to 2024.

## Contribution

The paper identifies emerging research hotspots and critical frontiers in lipid metabolism related to liver cancer.

## Key findings

- Research activity in lipid metabolism for liver cancer has surged, with over half of the literature published in the last three years.
- China and the USA are leading contributors, with the University of California System and the journal Cancers being the most prolific.
- Key future research areas include PPARγ, farnesoid X receptor, and NF-κB signaling in lipid metabolism and liver cancer.

## Abstract

This study aims to systematically map the intellectual landscape and emerging trends in lipid metabolism research within hepatocellular carcinoma from 2014 to 2024.

A total of 607 peer-reviewed publications were retrieved from the Web of Science Core Collection and PubMed. Bibliometric and visualization tools, including VOSviewer and CiteSpace, were employed to perform data analysis, including keyword co-occurrence and cluster analysis.

We identified a significant surge in research activity, with 53.05% of the total literature published in the last three years. China and the USA emerged as the leading contributors, with the University of California System and the journal Cancers being the most prolific institution and publication outlet, respectively. Current research hotspots are centered on the mechanisms by which oxidative stress drives the transformation of non-alcoholic fatty liver disease into hepatocellular carcinoma. Furthermore, three critical frontiers for future investigation were identified: (1) the regulatory role of PPARγ in lipid metabolic reprogramming and its therapeutic implications; (2) the molecular mechanisms of the farnesoid X receptor in modulating bile acid metabolism during hepatocarcinogenesis; and (3) the NF-κB signaling pathways that mediate metabolic shifts and confer chemoresistance in liver cancer.

These findings provide a comprehensive reference for prioritizing research directions and therapeutic target discovery in the metabolic-related oncology domain.

## Linked entities

- **Genes:** PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790]
- **Diseases:** hepatocellular carcinoma (MONDO:0007256), non-alcoholic fatty liver disease (MONDO:0013209)

## Full-text entities

- **Genes:** PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468] {aka CIMT1, FPLD3, GLM1, NR1C3, PPARG1, PPARG2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}
- **Diseases:** hepatocellular carcinoma (MESH:D006528), non-alcoholic fatty liver disease (MESH:D065626), Cancers (MESH:D009369)
- **Chemicals:** lipid (MESH:D008055), bile acid (MESH:D001647)

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13043338/full.md

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Source: https://tomesphere.com/paper/PMC13043338