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Microplastics/nanoplastics contribute to aging and age-related diseases: Mitochondrial dysfunction as a crucial role
Summary
This review examines how microplastics and nanoplastics may contribute to aging and age-related conditions by damaging mitochondria, the energy-producing structures inside cells. Researchers describe how these tiny plastic particles enter the body through food, water, and air, and accumulate in various organs where they can disrupt normal mitochondrial function. The study suggests that microplastic-driven mitochondrial damage could be an underappreciated factor in the aging process and related health decline.
The pervasive utilization of plastic products has led to a significant escalation in plastic waste accumulation. Concurrently, the implications of emerging pollutants such as microplastics (MPs) and nanoplastics (NPs) on human health are increasingly being acknowledged. Recent research has demonstrated that MPs/NPs may contribute to the onset of human aging and age-related diseases. Additionally, MPs/NPs have the potential to induce mitochondrial damage, resulting in mitochondrial dysfunction. Mitochondrial dysfunction is widely recognized as a hallmark of aging; thus, it is necessary to elucidate the relationship between them. In this article, we first elucidate the distribution of MPs/NPs in various environmental media, their pathways into the human body, and their subsequent distribution within human tissues and organs. Subsequently, we examine the interplay between MPs/NPs, mitochondrial dysfunction, and the aging process. We aspire that this article will enhance awareness regarding the toxicity of MPs/NPs while also offering a theoretical framework to support the development of improved regulatory policies in the future.
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