AI Article Synopsis

  • Exposure to air pollution leads to around seven million premature deaths and significantly contributes to disability, with particulate matter (PM) being a primary pollutant.
  • PM2.5, due to its large surface area, can absorb harmful substances and cause cellular issues like oxidative stress, inflammation, and apoptosis.
  • Non-coding RNAs (ncRNAs) are increasingly recognized for their role in responding to environmental changes, with exposure to PM2.5 linked to alterations in these ncRNAs, impacting health and disease processes.

Article Abstract

Exposure to air pollution has been connected to around seven million early deaths annually and also contributing to higher than 3 % of disability-adjusted lost life years. Particulate matters (PM) are among the key pollutants that directly discharged or formed due to atmospheric chemical interactions. Among these matters, due of its large surface area, PM2.5 may absorb a different harmful and toxic substances. One of the outcomes of such environmental disturbance is oxidative stress which affects cellular processes including apoptosis, inflammation, and epithelial mesenchymal transition. Non-coding RNAs (ncRNA) such as, miRNAs, lncRNAs, and circRNAs are classified as non-protein coding RNA's. Over the past few years these small molecules have been gaining so much attention since they participate in variety of physiological and pathological processes and their expression change during disease periods. Regarding epigenetic properties, ncRNAs play an important function in organism's response to environmental stimulus. In this manner, it was revealed that exposure to PM2.5 may cause epigenetic reprogramming, such as, ncRNAs signature's alteration, which can be effective concerning pathophysiology state. In this review, we describe PM2.5 impact on ncRNAs and excavate its roles in toxicity caused by PM2.5.

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Source
http://dx.doi.org/10.1016/j.ijbiomac.2023.123790DOI Listing

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