Caffeine, especially in coffee, can improve cell function in this life-threatening autoimmune condition.
A recent study examined the potential of caffeine to effectively fight against endothelial dysfunction in patients diagnosed with systemic lupus erythematosus (SLE). SLE is a complex autoimmune disease that affects various organs and can be life-threatening. The research, published in Rheumatology, explored how caffeine might specifically improve the function of endothelial progenitor cells (EPCs), specialized cells that help repair and maintain blood vessels by promoting the formation of new endothelial cells.
The study involved 31 patients with SLE, most of whom were females around the age of 43, and had been living with the disease for a median of 18 months. These individuals did not have other risk factors for cardiovascular disease such as high cholesterol or unhealthy lifestyle habits like smoking. Researchers used a food frequency questionnaire to determine the patients’ caffeine intake, focusing on coffee as the primary source.
One of the significant findings of the study was the link between caffeine intake and the percentage of EPCs in the bloodstream. Those with higher caffeine consumption had a higher percentage of circulating EPCs, indicating that caffeine may aid in the body’s ability to repair damaged blood vessels. This was particularly important because SLE often leads to heart issues, and those undergoing glucocorticoid treatment or suffering from neuropsychiatric lupus had notably lower EPC percentages.
The study went a step further by investigating how caffeine could reverse the harmful effects of SLE on healthy EPCs in a lab setting. When researchers exposed healthy EPCs to serum from SLE patients, the cells showed reduced colony formation and abnormal morphology. However, after caffeine was introduced at two different concentrations, the EPCs’ structure and function improved. This suggested that caffeine might counteract the negative effects of SLE on cardiovascular health.
Autophagy, a process where the body clears out damaged cells to make room for new ones, was also examined. In the presence of SLE serum, autophagy in the EPCs was impaired, as shown by the reduced levels of the molecule LC3-II and an increase in the molecule p62. Caffeine was able to restore these levels to normal, indicating that caffeine might help restore proper autophagy in SLE patients. This is important because autophagy plays a key role in maintaining cardiovascular health and ensuring that new blood vessels can form.
The researchers also explored how caffeine influenced apoptosis, or programmed cell death, in the EPCs. When the cells were exposed to SLE serum, apoptosis levels increased, as shown by higher levels of Annexin V, a marker for cell death. However, caffeine reduced these levels, suggesting that it could help protect EPCs from dying prematurely. This protective effect was also evident in the restoration of Bcl-2, a protein that helps prevent cell death, which had been reduced in cells treated with SLE serum.
SLE serum had caused an increase in A2AR levels and a reduction in SIRT3 and AMPK activity, both of which are important for maintaining cardiovascular health. However, caffeine restored these levels to normal, suggesting that this pathway could be the key to caffeine’s protective effects on blood vessels.
The findings of this study align with previous research showing that caffeine can protect against oxidative stress, which is known to accelerate the aging of cells. By activating the A2AR/SIRT3/AMPK pathway, caffeine seems to help EPCs survive longer, sustain their function, and prevent premature cell death, which is all important to maintaining a healthy cardiovascular system, particularly in patients with SLE, who are at higher risk for endothelial dysfunction.
While further research is still needed to confirm the team’s initial findings, the results of this preliminary study point to a potential new avenue for improving the health and quality of life of SLE patients.
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