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Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain
Background: Physical stressors can cause a physiological response that can contribute to an increase in mitochondrial dysfunction and Mitochondrial DNA damage (mtDNA damage). People living with HIV (PWH) are more likely to suffer from chronic pain and may be more susceptible to mitochondrial dysfunc...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10467217/ https://www.ncbi.nlm.nih.gov/pubmed/37542365 http://dx.doi.org/10.1177/17448069231195975 |
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author | Gilstrap, Shannon R Hobson, Joanna M Owens, Michael A White, Dyan M Sammy, Melissa J Ballinger, Scott Sorge, Robert E Goodin, Burel R |
author_facet | Gilstrap, Shannon R Hobson, Joanna M Owens, Michael A White, Dyan M Sammy, Melissa J Ballinger, Scott Sorge, Robert E Goodin, Burel R |
author_sort | Gilstrap, Shannon R |
collection | PubMed |
description | Background: Physical stressors can cause a physiological response that can contribute to an increase in mitochondrial dysfunction and Mitochondrial DNA damage (mtDNA damage). People living with HIV (PWH) are more likely to suffer from chronic pain and may be more susceptible to mitochondrial dysfunction following exposure to a stressor. We used Quantitative Sensory Testing (QST) as an acute painful stressor in order to investigate whether PWH with/without chronic pain show differential mitochondrial physiological responses. Methods: The current study included PWH with (n = 26), and without (n = 29), chronic pain. Participants completed a single session that lasted approximately 180 min, including QST. Blood was taken prior to and following the QST battery for assays measuring mtDNA damage, mtDNA copy number, and mtDNA damage-associated molecular pattern (DAMP) levels (i.e., ND1 and ND6). Results: We examined differences between those with and without pain on various indicators of mitochondrial reactivity following exposure to QST. However, only ND6 and mtDNA damage were shown to be statistically significant between pain groups. Conclusion: PWH with chronic pain showed greater mitochondrial reactivity to laboratory stressors. Consequently, PWH and chronic pain may be more susceptible to conditions in which mitochondrial damage/dysfunction play a central role, such as cognitive decline. |
format | Online Article Text |
id | pubmed-10467217 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-104672172023-08-31 Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain Gilstrap, Shannon R Hobson, Joanna M Owens, Michael A White, Dyan M Sammy, Melissa J Ballinger, Scott Sorge, Robert E Goodin, Burel R Mol Pain Research Article Background: Physical stressors can cause a physiological response that can contribute to an increase in mitochondrial dysfunction and Mitochondrial DNA damage (mtDNA damage). People living with HIV (PWH) are more likely to suffer from chronic pain and may be more susceptible to mitochondrial dysfunction following exposure to a stressor. We used Quantitative Sensory Testing (QST) as an acute painful stressor in order to investigate whether PWH with/without chronic pain show differential mitochondrial physiological responses. Methods: The current study included PWH with (n = 26), and without (n = 29), chronic pain. Participants completed a single session that lasted approximately 180 min, including QST. Blood was taken prior to and following the QST battery for assays measuring mtDNA damage, mtDNA copy number, and mtDNA damage-associated molecular pattern (DAMP) levels (i.e., ND1 and ND6). Results: We examined differences between those with and without pain on various indicators of mitochondrial reactivity following exposure to QST. However, only ND6 and mtDNA damage were shown to be statistically significant between pain groups. Conclusion: PWH with chronic pain showed greater mitochondrial reactivity to laboratory stressors. Consequently, PWH and chronic pain may be more susceptible to conditions in which mitochondrial damage/dysfunction play a central role, such as cognitive decline. SAGE Publications 2023-08-30 /pmc/articles/PMC10467217/ /pubmed/37542365 http://dx.doi.org/10.1177/17448069231195975 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Research Article Gilstrap, Shannon R Hobson, Joanna M Owens, Michael A White, Dyan M Sammy, Melissa J Ballinger, Scott Sorge, Robert E Goodin, Burel R Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain |
title | Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain |
title_full | Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain |
title_fullStr | Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain |
title_full_unstemmed | Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain |
title_short | Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain |
title_sort | mitochondrial reactivity following acute exposure to experimental pain testing in people with hiv and chronic pain |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10467217/ https://www.ncbi.nlm.nih.gov/pubmed/37542365 http://dx.doi.org/10.1177/17448069231195975 |
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