Scholarlink

Background <p>Epidemiological studies link pollution to higher coronary artery disease (CAD) risk, but the molecular pathways remain unclear. Mitochondria may play a role due to their sensitivity to pollutants. This study assesses the impact of air pollution on mitochondrial DNA copy number (mtDNAcn) in patients with angiographically documented CAD.</p> Methods <p>We performed a prospective single-center cohort design by enrolling 151 patients undergoing coronary angiography in the Milan area: 89 with acute coronary syndrome (ACS), and 62 with chronic coronary syndrome (CCS). Daily levels of PM<sub>2.5,</sub> PM<sub>10</sub>, and meteorological data were collected from fixed monitoring stations. Exposure was averaged over short- (1&#xa0;week, 2&#xa0;weeks, 3&#xa0;weeks and 1&#xa0;month) and long-term (1&#xa0;year) periods before angiography. mtDNAcn, was measured by real-time PCR. Systemic inflammatory index (SII) was calculated from the complete blood count.</p> Results <p>ACS patients were exposed to significantly higher short-term levels of PM<sub>2.5</sub> and PM<sub>10</sub> and a greater number of days exceeding their recommended annual limits, compared to the CCS group. Multivariable linear regression showed that short-term exposure to PM<sub>2.5</sub> and PM<sub>10</sub> was inversely associated with mtDNAcn in ACS. Specifically, an interquartile range increase of 21.02&#xa0;µg/m<sup>3</sup> in 3-week PM<sub>2.5</sub>, 19.13&#xa0;µg/m<sup>3</sup> in 1-month PM<sub>2.5</sub>, and 23.03&#xa0;µg/m<sup>3</sup> in 1-month PM<sub>10</sub> was associated with decreases in mtDNAcn of 28.00%, 29.51%, and 17.36%, respectively. mtDNAcn also negatively correlated with SII (<i>P</i> = 0.028) in the study population.</p> Conclusions <p>Short-term exposure to PM<sub>2.5</sub> and PM<sub>10</sub> is associated to reduce mtDNAcn in ACS., supporting a potential role of mitochondrial dysfunction in the pathogenesis of acute events and plaque vulnerability.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Short-term exposures to air pollutants affect mitochondrial DNA copy number in patients with acute but not in chronic coronary syndromes

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月27日

查看全文
  • Gianluca Gazzaniga,
  • Paola Canale,
  • Marina Parolini,
  • Cinzia Dellanoce,
  • Emanuela Piccaluga,
  • Irene Bossi,
  • Claudio Montalto,
  • Jacopo Andrea Oreglia,
  • Maria Grazia Andreassi,
  • Jonica Campolo

摘要

Background

Epidemiological studies link pollution to higher coronary artery disease (CAD) risk, but the molecular pathways remain unclear. Mitochondria may play a role due to their sensitivity to pollutants. This study assesses the impact of air pollution on mitochondrial DNA copy number (mtDNAcn) in patients with angiographically documented CAD.

Methods

We performed a prospective single-center cohort design by enrolling 151 patients undergoing coronary angiography in the Milan area: 89 with acute coronary syndrome (ACS), and 62 with chronic coronary syndrome (CCS). Daily levels of PM2.5, PM10, and meteorological data were collected from fixed monitoring stations. Exposure was averaged over short- (1 week, 2 weeks, 3 weeks and 1 month) and long-term (1 year) periods before angiography. mtDNAcn, was measured by real-time PCR. Systemic inflammatory index (SII) was calculated from the complete blood count.

Results

ACS patients were exposed to significantly higher short-term levels of PM2.5 and PM10 and a greater number of days exceeding their recommended annual limits, compared to the CCS group. Multivariable linear regression showed that short-term exposure to PM2.5 and PM10 was inversely associated with mtDNAcn in ACS. Specifically, an interquartile range increase of 21.02 µg/m3 in 3-week PM2.5, 19.13 µg/m3 in 1-month PM2.5, and 23.03 µg/m3 in 1-month PM10 was associated with decreases in mtDNAcn of 28.00%, 29.51%, and 17.36%, respectively. mtDNAcn also negatively correlated with SII (P = 0.028) in the study population.

Conclusions

Short-term exposure to PM2.5 and PM10 is associated to reduce mtDNAcn in ACS., supporting a potential role of mitochondrial dysfunction in the pathogenesis of acute events and plaque vulnerability.