Microcystin-LR hijacks mitochondrial bioenergetics and Wnt crosstalk: Unveiling a novel dual-pathway mechanism for adipogenesis dysregulation in environmental toxicology.
Duan W., Yang T., Liu W., Zhan C.
Animal Study, published in Comp Biochem Physiol C Toxicol Pharmacol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Comp Biochem Physiol C Toxicol Pharmacol (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40818727
- DOI
- 10.1016/j.cbpc.2025.110329
Abstract (original English)
Cyanobacterial blooms, driven by toxin-producing cyanobacteria, pose significant environmental health risks due to the persistent release of cyanotoxins like microcystin-LR (MC-LR). While much research has focused on its hepatotoxic, nephrotoxic, and neurotoxic effects, its impact on adipose tissue homeostasis remains poorly understood. This study investigates the effects of MC-LR on stromal vascular fraction (SVF) cells, key progenitors in adipogenesis and metabolic regulation. Using cell culture models, we examine mitochondrial dysfunction and Wnt/β-catenin signaling pathway as two primary mechanisms of MC-LR-induced adipose dysfunction. Our findings show that MC-LR exposure leads to ATP depletion, ROS accumulation, impaired oxidative phosphorylation, and mitophagy activation, which collectively suppress lipogenesis. Additionally, MC-LR activates Wnt/β-catenin signaling pathway, disrupting adipogenesis regulatory pathways. These mechanisms interact in a self-reinforcing cycle of adipocyte dysfunction, linking mitochondrial failure to Wnt/β-catenin pathway hyperactivation. This study is the first to systematically elucidate the molecular mechanisms by which MC-LR disrupts adipogenesis in SVF cells, providing critical insights into the role of cyanotoxins in modulating human adipogenesis and obesity-related metabolic dysregulation.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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