Evidence mapPaperPMID 41582137Full record

ReviewLipids in health and disease2026

Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk.

Qiqi Zhao, Shengwen Lu, Yu Guan, Zhiwen Sun, Shi Qiu, Aihua Zhang

Abstract readReview
In one paragraph

Review in Lipids in health and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Total Flavonoids fromAntioxidants (Basel, Switzerland) · 2026
    Article
  2. 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

6 authors.

Qiqi ZhaoGAP Center, Department of Pharmaceutical Analysis, School of Basic Medicine, Graduate School, Heilongjiang University of Chinese Medicine, Heping Road 24, Harbin, 150040, China.
Shengwen LuGAP Center, Department of Pharmaceutical Analysis, School of Basic Medicine, Graduate School, Heilongjiang University of Chinese Medicine, Heping Road 24, Harbin, 150040, China.
Yu GuanGAP Center, Department of Pharmaceutical Analysis, School of Basic Medicine, Graduate School, Heilongjiang University of Chinese Medicine, Heping Road 24, Harbin, 150040, China.
Zhiwen SunDepartment of Gastroenterology, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Heping Road 24, Harbin, 150040, China.
Shi QiuInternational Advanced Functional Omics Platform, School of Chinese Medicine, Scientific Experiment Center, Hainan Medical University, Xueyuan Road 3, Haikou, 571199, China.
Aihua ZhangGAP Center, Department of Pharmaceutical Analysis, School of Basic Medicine, Graduate School, Heilongjiang University of Chinese Medicine, Heping Road 24, Harbin, 150040, China. aihuatcm@163.com.ORCID http://orcid.org/0000-0002-3784-4472

Funding

Program of Natural Science Foundation of State 81703686Program of Natural Science Foundation of State 81973745Traditional Chinese Medicine Research Project on Traditional Chinese Medicine of Heilongjiang Province ZHY2025-112University Nursing Program for Young Scholars with Creative Talents in Heilongjiang Province UNPYSCT-2018221
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD), whose pathogenesis involves complex multi-organ crosstalk and the remodeling of the hepatic immune microenvironment, constitutes a major global health challenge. The latest research indicates that the dysregulation of the AMPK-SREBP1-FASN (ASF) signaling axis plays a core role in mediating abnormal fatty acid synthesis and the accumulation of lipotoxic metabolites in MASLD, serving as a key molecular hub linking hepatic metabolic disorders with immune inflammatory responses. Dysregulated ASF axis and the subsequent lipotoxic products not only directly impair hepatocellular organelle function but also, by disrupting intercellular communication and reprogramming immune cell and hepatocyte metabolism, drive a self-perpetuating “metabolic-immune” vicious cycle. This cycle propels disease progression toward fibrosis and extrahepatic complications. However, how ASF axis dysregulation specifically reshapes the hepatic immune landscape remains to be systematically elucidated. This review aims to systematically describe the crucial role of the ASF axis in MASLD. First, it outlines the pivotal function of this axis in multi-system interactions and the disruption of the hepatic immune microenvironment. It then provides an in-depth analysis of the regulatory mechanisms and functional characteristics of the ASF axis in both hepatocytes and immune cells. Furthermore, it explores the molecular mechanisms by which ASF axis dysregulation exacerbates lipotoxicity through promoting CD36-dependent lipid uptake and dissects how lipotoxicity impairs hepatocellular function and hepatic immune homeostasis in MASLD. Finally, the review summarizes potential therapeutic strategies targeting the ASF axis, which are designed to disrupt the metabolic-immune vicious cycle and restore systemic homeostasis. By offering an integrated perspective, this review seeks to advance the understanding of the immune-metabolic pathogenesis of MASLD and to establish a theoretical foundation for developing precise therapeutic interventions.

Indexed as

AMP-Activated Protein KinasesFatty LiverSterol Regulatory Element Binding Protein 1AnimalsHepatocytesHumansLipid MetabolismLiverSignal TransductionAMP-Activated Protein KinasesSREBF1 protein, humanSterol Regulatory Element Binding Protein 1AMPK- SREBP1- FASN axisLipotoxicity.MASLDMetabolic-immune cycleMicroenvironment

Identifiers

PMID41582137
PMCPMC12918582

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.