We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Cadmium disrupts hepatic lipid homeostasis: molecular mechanisms, unresolved controversies, and therapeutic strategies
AI summary Read the abstract
This review systematically examined how cadmium accumulates in the liver and disrupts hepatic lipid metabolism, covering mechanisms including mitochondrial dysfunction, oxidative stress, and lipid droplet accumulation. The authors also reviewed therapeutic strategies and identify persistent knowledge gaps in cadmium hepatotoxicology.
Cadmium, a pervasive environmental toxicant with profound bioaccumulation potential, poses a significant threat to hepatic lipid homeostasis. This review systematically delineates the intricate molecular mechanisms underlying the cadmium-induced dysregulation of hepatic lipid metabolism. We highlight that cadmium accumulation in the liver triggers a cascade of pathological events, including mitochondrial dysfunction, aberrant activation of nuclear receptors driving lipogenesis, and epigenetic reprogramming. Concurrently, cadmium exacerbates oxidative stress, amplifies inflammatory cascades, and disrupts the gut-liver axis. Critically, unresolved controversies such as the dual effects on liver lipid homeostasis under chronic environmental cadmium exposure, sexual dimorphism in susceptibility (potentially estrogen-mediated), and synergistic hepatotoxicity from co-exposure with microplastics are discussed. We further explore emerging therapeutic strategies targeting these pathways, including antioxidant therapy, epigenetic modulation, and microbiota-based interventions. This synthesis clarifies the mechanistic pathways linking cadmium exposure to hepatic lipid accumulation and identifies critical research gaps for future investigation.
More Papers Like This
Molecular regulatory networks of microplastics and cadmium mediated hepatotoxicity from NAFLD to tumorigenesis via integrated approaches
AI summary Read the abstract
This study mapped out how microplastics and the toxic metal cadmium work together to damage the liver, tracing a progression from fatty liver disease to cirrhosis and eventually liver cancer. Cadmium activates genes linked to cell growth and tumor formation, while microplastics trigger cell death pathways related to inflammation. When combined, the two pollutants accelerate liver damage more than either one alone, raising concerns about real-world exposure where people encounter both simultaneously.
Cell organelles as targets of mammalian cadmium toxicity
AI summary Read the abstract
This review examines how cadmium — an industrial heavy metal increasingly present in soil, water, and food — damages cell organelles including mitochondria, lysosomes, the nucleus, and the endoplasmic reticulum, with connections to microplastics as a delivery vector for cadmium exposure.
Environmental microplastics and liver health: Brief review on human exposure and accumulation, hepatotoxicity mechanism, and intervention strategies
AI summary Read the abstract
This review links human exposure to microplastics, their accumulation in the liver and proposed mechanisms of liver toxicity, including oxidative stress, inflammation and cell death. Most of the evidence comes from cell, animal and organoid studies. It also discusses candidate interventions that are still at the research stage.
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
AI summary Read the abstract
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
AI summary Read the abstract
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.