Smoking is Associated with Remodeling of Gap Junction in the Rat Heart: Smoker's Paradox Explanation?

Abstract

Exposure to tobacco smoke resulted in cardiac gap junction remodeling, characterized by alterations in the quantity and phosphorylation of the Cx43, in rats hearts. This finding could explain the smoker's paradox observed in some studies.

CX43 Expression in Colonic Adenomas and Surrounding Mucosa Is a Marker of Malignant Potential

“…We did not find any correlation of CX43 expression in adenomas and colonic mucosa with history of smoking as an earlier study suggested (23).…”

“Smoker’s Paradox” in Patients Treated for Severe Injuries: Lower Risk of Mortality After Trauma Observed in Current Smokers

“…In the cardiology literature, many studies support the idea that long-term physiological changes in endothelial and cardiac tissue explain the smoking paradox. 12,14 Undoubtedly smoking does cause enduring physical changes in organ systems, however, Hung et al 30 reported that smokers also experience acute platelet activation in as little as 5 minutes after smoking a cigarette. Schmidt and Rasmussen 41 also reported a similar fast-acting effect on platelet activation in nonsmokers after smoking a cigarette.…”

“…However, laboratory studies have proposed that changes in endothelial function, enhanced thrombolysis, induced inflammation, faster epicardial flow, and remodeling of cardiac gap junctions are plausible explanations for the smoking paradox. [10][11][12][13][14] In the trauma setting, the effect of smoking status on mortality outcomes in trauma patients has not been well studied. 15 Considering that both traumatic injury and acute cardiac events' lethality often results from inadequate levels of oxygen delivery and utilization at the cellular level, the survival benefit of smoking on mortality outcomes in cardiac patients may be present in the injured patient population as well.…”

Impact of baseline cigarette smoking status on clinical outcome after transcatheter aortic valve replacement

“…46 Furthermore, multiple preclinical and clinical studies confirmed the paradoxical effect of smoking on outcome after AMI and among patients undergoing elective PCI, and attributed the beneficial effects to cardiac gap junction remodeling and ischemic preconditioning. [47][48][49] Moreover, smokers compared with never-smokers may have faster epicardial flow as measured by angiography, 50 less target lesions revascularization, 51 and lower cardiac troponin level which is an indicators for cardiac damage. 52 In addition, it has been suggested that smoker's paradox exist duo to the fact that smokers have a greater thrombus burden leading to greater efficacy of thrombolytic therapy and antiplatelet therapy.…”