Lipotoxicity in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Its Therapeutic Control
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 31 January 2026 | Viewed by 53
Special Issue Editor
Interests: amino acid metabolism; homocysteine; hydrogen sulfide; PPAR; lipid signaling; metabolic diseases
Special Issues, Collections and Topics in MDPI journals
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Dear Colleagues,
The numbers of patients with metabolic dysfunction–associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), are increasing significantly worldwide. However, in contrast to the multiple drugs available for treating type 2 diabetes, another metabolic disease related to obesity, there are no effective therapeutics for MASLD, except for Resmetirom, a thyroid hormone receptor-beta (THR-β) agonist approved by the FDA on March 14, 2024.
Most forms of MASLD feature benign fatty liver, known as metabolic dysfunction–associated fatty liver (MAFL). The remaining 20% of MASLD cases progress to metabolic dysfunction–associated steatohepatitis (MASH), which is defined by diagnoses of steatosis, hepatocyte ballooning, and lobular inflammation with and without fibrosis. An estimated 20% of patients with MASH will develop cirrhosis, for which no cure is available. Under these current conditions, peroxisome proliferator-activated receptor (PPAR) or farnesoid X receptor (FXR) agonists—which induce expression of anti-inflammatory and antioxidant genes and suppress oxidative stress and associated lipotoxicity in the early stage of progression to MASH—are expected to be new therapeutic options. Oxidative stress is considered as one of the key factors in progression to MASH because the excessive formation of reactive lipid aldehydes, such as 4-hydroxy-2-nonenal (4-HNE), malondialdehyde (MDA), and acrolein, via Fenton reaction beyond the surrounding antioxidant milieu, induces the carbonylation of cysteine, histidine, and lysine residues of functional proteins, which could lead to adduct-/antigen-driven inflammation and fibrosis.
This Special Issue of Antioxidants aims to share new experimental results and ideas that contribute to the understanding of lipotoxicity in MASLD and the development or repurposing of drugs for preventing and treating MASLD.
Prof. Dr. Isao Ishii
Guest Editor
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Keywords
- metabolic dysfunction–associated steatotic liver disease (MASLD)
- metabolic dysfunction–associated steatohepatitis (MASH)
- fatty liver
- lipotoxicity
- ferroptosis
- inflammation
- fibrosis
- Fenton reaction
- thyroid hormone receptor-beta (THR-β) agonist
- peroxisome proliferator-activated receptor (PPAR) agonist
- farnesoid X receptor (FXR) agonist
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