The 2025 American Association for the Study of Liver Disease (AASLD) annual meeting, The Liver Meeting, recently concluded. The five-day event, which ran from November 7 through November 11, featured thousands of research presentations, insightful sessions, and exciting networking opportunities. 

For your convenience, we have a curated selection of some of the many abstracts that focus on metabolic dysfunction-associated steatohepatitis (MASH) and MASH-related research, along with their associated descriptions and conclusions. Some descriptions and conclusions were edited for brevity and clarity. To view all of the abstracts presented at the AASLD Annual Meeting, the 2025 Abstract Supplement is available online. Please note that this is a very large .pdf file, so a strong internet connection is recommended. 

2025 AASLD Annual Meeting Abstracts Relating to MASH

Genetic or Pharmacological Inhibition of Hepatic TMEM141 Attenuates MASH and Fibrosis via the ROSHNF4α Signaling Pathway

  • Description: Researchers presented a protein, transmembrane protein 141, with a largely unknown function, as a key regulator of MASH and MASH-associated fibrosis. 
  • Conclusion: The findings highlight a key role of transmembrane protein 141 in MASH development, suggesting targeting hepatic transmembrane protein 141 may be a novel strategy for treating MASH and MASH-associated fibrosis.

Nuclear Translocation of D-2-Hydroxyglutarate Dehydrogenase (D2HGDH) Drives Progression of Metabolic Dysfunction-Associated Steatohepatitis (MASH)

  • Description: Metabolic dysfunction-associated steatohepatitis (MASH) represents an advanced stage of metabolic dysfunction-associated steatotic liver disease characterized by hepatic steatosis, inflammation, and progressive fibrosis.
  • Conclusion: Nuclear D2HGDH and cytosolic D-2-HG create a feedforward loop—nuclear 2-OG drives epigenetic lipogenesis, while secreted D-2HG exacerbates intercellular fibrosis and inflammation, defining a metabolite-centric mechanism in MASH pathogenesis.

TOX3 Promotes MASH Progression by Regulating Hepatic A-Linolenic Acid Metabolism via the PI3K/Akt Signaling Pathway

  • Description: Researchers sought to delineate the mechanistic contributions of TOX3 to MASH progression and evaluate its therapeutic potential.
  • Conclusion: Researchers established TOX3 as a critical regulator of MASH pathogenesis through PI3K/Akt-mediated coupling of lipid metabolism and inflammatory cascades.

Intestinal Lipase Inhibition Prevents Obesity But Exacerbates MASH

  • Description: [The research team’s] previous work demonstrated that polyunsaturated fatty acids (PUFAs) are preferentially absorbed over saturated fats to maintain metabolic homeostasis. However, orlistat, a lipase inhibitor used for weight loss, disrupts this selective uptake on a Western-style diet, leading to hepatic PUFA depletion.
  • Conclusion: Orlistat, despite its anti-obesity effects, aggravates liver injury in the context of MASH. Orlistat’s therapeutic potential and risk appear to depend on the fat content of the diet, underscoring the significance of dietary fat composition in strategies that target lipid absorption.

Salidroside Alleviates MASH Through PPARγ-Mediated Inflammatory Signaling Pathway

  • Description: Salidroside, a bioactive compound from Rhodiola rosea, exhibits anti-inflammatory and metabolic regulatory properties, but its mechanism in MASH remains unclear.
  • Conclusion: Researchers found that salidroside ameliorates MASH by activating PPARγ, thereby inhibiting NF-κB-mediated inflammation and hepatic lipid accumulation.

Development and Validation of Qinflammation: An AI-Driven Digital Pathology Algorithm for Differentiating Portal and Lobular Inflammation in Metabolic-Associated Steatohepatitis

  • Description: This study describes the first-round development and performance of the qInflammation (qI) algorithm, with two additional optimization rounds planned.
  • Conclusion: The first-round evaluation demonstrates qI’s robust potential for automated quantification of portal/lobular inflammation in MASH.

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