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A systematic review on the impact of fine particulate matter on bone marrow-stored hematopoietic and mesenchymal stem cells

Title: The Impact of Fine Particulate Matter on Bone Marrow-Stored Hematopoietic and Mesenchymal Stem Cells: A Systematic Review

Introduction:
Fine particulate matter (PM2.5) refers to tiny particles suspended in the air, with a diameter of 2.5 micrometers or smaller. These particles are released into the atmosphere through various sources such as vehicle emissions, industrial processes, and burning of fossil fuels. Over the past few decades, there has been growing concern about the adverse health effects of PM2.5 exposure, particularly its impact on respiratory and cardiovascular systems. However, emerging evidence suggests that PM2.5 may also have detrimental effects on bone marrow-stored hematopoietic and mesenchymal stem cells, which play a crucial role in maintaining the body’s immune system and regenerative capacity.

Methods:
To explore the impact of PM2.5 on bone marrow-stored hematopoietic and mesenchymal stem cells, a systematic review was conducted. Relevant studies were identified through comprehensive searches of electronic databases, including PubMed, Scopus, and Web of Science. The search terms included “fine particulate matter,” “PM2.5,” “stem cells,” “hematopoietic stem cells,” and “mesenchymal stem cells.” Only studies published in English and conducted on human or animal models were included.

Results:
The systematic review identified several studies investigating the effects of PM2.5 exposure on bone marrow-stored stem cells. These studies utilized various experimental models, including in vitro cell cultures, animal models, and human population-based studies. The findings collectively suggest that PM2.5 exposure can have detrimental effects on both hematopoietic and mesenchymal stem cells.

Hematopoietic Stem Cells:
Several studies have demonstrated that PM2.5 exposure can lead to alterations in hematopoietic stem cell function. It has been observed that PM2.5 exposure can induce oxidative stress, inflammation, and DNA damage in hematopoietic stem cells, impairing their ability to differentiate into mature blood cells. Additionally, PM2.5 exposure has been associated with decreased hematopoietic stem cell proliferation and increased apoptosis, leading to a decline in the overall regenerative capacity of the immune system.

Mesenchymal Stem Cells:
Similarly, PM2.5 exposure has been shown to negatively impact mesenchymal stem cells. These cells are responsible for tissue repair and regeneration and play a crucial role in maintaining the integrity of various organs and tissues. Studies have reported that PM2.5 exposure can impair the differentiation potential of mesenchymal stem cells, leading to reduced regenerative capacity. Furthermore, PM2.5 exposure has been linked to increased oxidative stress and inflammation in mesenchymal stem cells, further compromising their regenerative abilities.

Mechanisms of Action:
The detrimental effects of PM2.5 on bone marrow-stored stem cells are thought to be mediated through various mechanisms. Oxidative stress, inflammation, and DNA damage have been identified as key pathways through which PM2.5 exerts its toxic effects on stem cells. Additionally, PM2.5 exposure can disrupt the bone marrow microenvironment, altering the signaling pathways necessary for stem cell maintenance and differentiation.

Conclusion:
This systematic review highlights the potential adverse effects of PM2.5 exposure on bone marrow-stored hematopoietic and mesenchymal stem cells. The findings suggest that PM2.5 exposure can impair the regenerative capacity of these stem cells, compromising the body’s immune system and tissue repair mechanisms. Further research is needed to elucidate the underlying mechanisms and develop strategies to mitigate the harmful effects of PM2.5 on stem cell function. Additionally, public health policies aimed at reducing PM2.5 levels are crucial to protect the population from the detrimental effects of air pollution on stem cell health and overall well-being.

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