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Publications

Journal Article Research Support, Non-U.S. Gov't Ppublish 4 citations

PubMed: 36567551 DOI: 10.1177/1358863X221143152

Cigarette smoking and mitochondrial dysfunction in peripheral artery disease.

Vasc Med 28(1):28-35

Authors: Michelle Guo, Mary M McDermott, Sudarshan Dayanidhi, Christiaan Leeuwenburgh, Stephanie Wohlgemuth, Luigi Ferrucci, Charlotte A Peterson, Kate Kosmac, Lu Tian, Lihui Zhao, Robert Sufit, Karen Ho, Michael Criqui, Shujun Xu, Dongxue Zhang, Philip Greenland

Affiliations

  • Department of Medicine, Northwestern University, Chicago, IL, USA.
  • Department of Preventive Medicine, Northwestern University, Chicago, IL, USA.
  • Shirley Ryan AbilityLab, Northwestern University, Chicago, IL, USA.
  • Department of Aging and Geriatric Research, University of Florida, Gainesville, FL, USA.
  • Division of Intramural Research, National Institute on Aging, Baltimore, MD, USA.
  • Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
  • Department of Health Research and Policy, Stanford University, Stanford, CA, USA.
  • Department of Neurology, Northwestern University, Chicago, IL, USA.
  • Department of Surgery, Northwestern University, Chicago, IL, USA.
  • Departments of Preventive Medicine, Family Medicine, and Public Health, University of California San Diego, San Diego, CA, USA.

Abstract

BACKGROUND

This study evaluated the association of smoking with mitochondrial function in gastrocnemius muscle of people with peripheral artery disease (PAD).

METHODS

Participants were enrolled from Chicago, Illinois and consented to gastrocnemius biopsy. Mitochondrial oxidative capacity was measured in muscle with respirometry. Abundance of voltage-dependent anion channel (VDAC) (mitochondrial membrane abundance), peroxisome proliferator-activated receptor-γ coactivator (PGC-1α) (mitochondrial biogenesis), and electron transport chain complexes I-V were measured with Western blot.

RESULTS

Fourteen of 31 people with PAD (age 72.1 years, ABI 0.64) smoked cigarettes currently. Overall, there were no significant differences in mitochondrial oxidative capacity between PAD participants who currently smoked and those not currently smoking (complex I+II-mediated oxidative phosphorylation: 86.6 vs 78.3 pmolO 2/s/mg, respectively [p = 0.39]). Among participants with PAD, those who currently smoked had a higher abundance of PGC-1α (p < 0.01), VDAC (p = 0.022), complex I (p = 0.021), and complex III (p = 0.021) proteins compared to those not currently smoking. People with PAD who currently smoked had lower oxidative capacity per VDAC unit (complex I+II-mediated oxidative phosphorylation [137.4 vs 231.8 arbitrary units, p = 0.030]) compared to people with PAD not currently smoking. Among people without PAD, there were no significant differences in any mitochondrial measures between currently smoking (n = 5) and those not currently smoking (n = 63).

CONCLUSIONS

Among people with PAD, cigarette smoking may stimulate mitochondrial biogenesis to compensate for reduced oxidative capacity per unit of mitochondrial membrane, resulting in no difference in overall mitochondrial oxidative capacity according to current smoking status among people with PAD. However, these results were cross-sectional and a longitudinal study is needed.

MeSH

Mitochondria, Arteries, Vascular Diseases, Muscles, Peroxisome Proliferator-Activated Receptors, Mitochondrial Membranes, Voltage-Dependent Anion Channels, Organelle Biogenesis, Peripheral Arterial Disease, Cigarette Smoking

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