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dc.creatorDella Guardia, Lucio
dc.creatorShin, Andrew C. (TTU)
dc.date.accessioned2022-05-12T18:38:38Z
dc.date.available2022-05-12T18:38:38Z
dc.date.issued2022
dc.identifier.citationDella Guardia, L., Shin, A.C. White and brown adipose tissue functionality is impaired by fine particulate matter (PM2.5) exposure. J Mol Med (2022). https://doi.org/10.1007/s00109-022-02183-6en_US
dc.identifier.urihttps://doi.org/10.1007/s00109-022-02183-6
dc.identifier.urihttps://hdl.handle.net/2346/89184
dc.descriptionThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.en_US
dc.description.abstractChronic exposure to high levels of particulate matter (PM) is correlated to a higher prevalence of cardio-metabolic disturbances. Adipose tissue represents a pivotal regulator of metabolic homeostasis, and its dysfunction is associated with health issues in PM-exposed models. This review discusses the adaptive changes of white (WAT) and brown (BAT) adipose tissue in response to fine particulate matter (PM2.5), investigating the underlying pathophysiology. In exposed models, PM2.5 increases oxidative stress and impairs mitochondria functionality and biogenesis in WAT and BAT. Chronic exposure also upregulates the main apoptotic/pro-inflammatory pathways and promotes the infiltration of monocytes and the accumulation of activated macrophages. Oxidative stress and inflammation are responsible for the inhibition of insulin signal transduction and glucose uptake in both the adipose tissues. The increased inflammatory status also suppresses the metabolic activity of brown adipocytes, promoting the whitening. Altogether, this evidence suggests the shift of WAT and BAT toward an inflammatory and metabolic dysfunctional phenotype. Although the underlying mechanisms remain to be clarified, the development of inflammation in lungs, gut, and hypothalamus seems to have a pivotal role in the alteration of adipose tissue homeostasis. The potential consequences on systemic cardio-metabolic health render the relationship PM-adipose tissue a key issue to investigate.en_US
dc.language.isoengen_US
dc.subjectAdipocytesen_US
dc.subjectAir Pollutionen_US
dc.subjectInflammationen_US
dc.subjectInsulin Resistanceen_US
dc.subjectMetabolic Diseasesen_US
dc.subjectMacrophagesen_US
dc.titleWhite and brown adipose tissue functionality is impaired by fine particulate matter (PM2.5) exposureen_US
dc.typeArticleen_US


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