Cigarette Smoke Damage in Blood Vessels Eased by Colchicine

Jim Crocker
6th April, 2024

Cigarette Smoke Damage in Blood Vessels Eased by Colchicine

Image Source: Natural Science News, 2024

Key Findings

  • Study at Heinrich-Heine-Universität Düsseldorf finds smoking induces cell aging and inflammation
  • Colchicine, a gout medication, can prevent these aging effects in blood vessel cells
  • Colchicine's action suggests a new way to treat smoking-related heart disease and cancer
Smoking, a well-known public health enemy, has been linked to an array of chronic diseases, particularly cardiovascular diseases and cancer. Researchers at Heinrich-Heine-Universität Düsseldorf have made a significant breakthrough in understanding how smoking exacerbates these conditions[1]. Their study zeroes in on the process of cellular senescence, a state where cells cease to divide and begin to secrete inflammatory substances, which can lead to tissue damage and disease progression. Cellular senescence is a complex biological process that serves as a double-edged sword. On one hand, it is a defense mechanism that prevents damaged cells from becoming cancerous[2]. On the other, it can contribute to aging and the development of age-related diseases when senescent cells accumulate[2][3]. These cells release various pro-inflammatory molecules and enzymes, such as matrix metalloproteinases, which degrade the proteins that give tissues their structure and can thus initiate cardiovascular diseases and aid cancer metastasis[4]. The Düsseldorf study investigated how exposure to tobacco smoke leads to oxidative stress—a situation where harmful oxygen-containing molecules cause damage to cells, including their DNA—and how this stress pushes cells into the senescent state. They found that endothelial cells, which line the interior surface of blood vessels, exposed to tobacco smoke condensate, showed increased signs of senescence. However, the study's breakthrough was the discovery that colchicine, a medication commonly used to treat gout, can effectively block the senescence of these endothelial cells. Colchicine was shown to prevent oxidative stress and DNA damage, two triggers of cellular senescence. It accomplished this by reducing the activity of β-galactosidase (β-gal), a marker of senescence, and by improving levels of Lamin B1, a structural protein that is often depleted in senescent cells. Furthermore, colchicine attenuated the levels of P21 and P53, proteins that are known to halt cell division and are associated with the onset of cellular senescence[2]. The study also demonstrated that colchicine could reduce the expression of senescence-associated secretory phenotype (SASP) factors—pro-inflammatory molecules secreted by senescent cells. This is particularly important because SASP can disrupt the tissue microenvironment and promote disease progression[2][4]. Colchicine's beneficial effects also extended to inhibiting the activation of NF-kB and MAPKs P38 and ERK, signaling molecules that play a role in inflammation and stress responses. By targeting these pathways, colchicine not only prevented the onset of senescence in endothelial cells exposed to tobacco smoke but also suggested a potential therapeutic avenue for smoking-related diseases. This aligns with previous findings that lifestyle factors, including tobacco consumption, can disrupt normal physiological balance and contribute to non-communicable diseases[3]. The current study adds to this body of knowledge by showing that colchicine can counteract some of the harmful effects of smoking on cells. In summary, the research from Heinrich-Heine-Universität Düsseldorf provides new insights into how smoking induces cellular senescence and offers a promising strategy for mitigating this effect. By using colchicine to block the senescence pathway, there is potential for developing treatments that could reduce the burden of cardiovascular diseases and cancer associated with smoking. This study not only advances our understanding of the pathophysiological impacts of smoking but also underscores the importance of identifying and targeting cellular mechanisms to prevent the onset of chronic diseases.



Main Study

1) Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation

Published 3rd April, 2024

Related Studies

2) Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype.

3) Pathogenesis of (smoking-related) non-communicable diseases-Evidence for a common underlying pathophysiological pattern.

4) A guide to assessing cellular senescence in vitro and in vivo.

Related Articles

An unhandled error has occurred. Reload 🗙