Fine particulate matter (PM2.5) is a serious environmental problem worldwide. It is known to increase the risk of various diseases by inducing oxidative stress and chronic inflammation. Although patients with Type 2 diabetes mellitus are especially vulnerable to environmental stress, the effects of fine particulate matter on bone marrow stem cells and the bone marrow microenvironment remain unclear.

This mechanism was proposed in a study by Professor Seong-Ho Guk's team at Jeonbuk National University (JBNU), Graduate School, Department of Bioactive Material Sciences, attracting attention from the academic community. Professor Guk's team reported research findings that elucidate the molecular mechanism by which the interaction between fine particulate matter and Type 2 diabetes mellitus promotes senescence and functional decline of bone marrow stem cells.

Professor Seong-Ho Guk and Professor Jeong-Chae Lee (School of Dentistry) and their research team used an atmospheric simulation chamber (Atmospheric Simulation Chamber) reproducing real atmospheric conditions and a Type 2 diabetes animal model. They confirmed that exposure to fine particulate matter further accelerates deterioration of bone marrow stem cell function in a diabetic environment.

The study found that increased oxidative stress and chronic inflammation associated with Type 2 diabetes mellitus transform the bone marrow microenvironment into an aged state and reduce the regenerative capacity of stem cells.

Moreover, additional exposure to fine particulate matter was found to further exacerbate senescence and functional decline of bone marrow stem cells.

In particular, fine particulate matter activates the NLRP3 inflammasome pathway in lung tissue, inducing a systemic inflammatory response. This process was analyzed as a key mechanism promoting senescence of bone marrow stem cells.

These changes were more pronounced in the Type 2 diabetes group than in the control group. Administration of an NLRP3 inhibitor significantly improved the functional decline and senescence of bone marrow stem cells.

This study has important academic significance in that it identified the molecular mechanism by which the environmental pollutant fine particulate matter and the metabolic disease Type 2 diabetes mellitus interact to impair bone marrow stem cell function.

At the same time, by indicating that the NLRP3 inflammasome is a central regulator of this pathophysiological process, the study is seen as opening new possibilities for protecting the health of chronic disease patients vulnerable to environmental pollution and for developing therapeutic strategies.

The research findings were published in the latest issue of the internationally respected environmental science journal Journal of Hazardous Materials (IF=10.6). The paper is titled 'Fine particulate matter accelerates the senescence of bone marrow-conserved stem cells in a type 2 diabetes mellitus mouse model.'

Professor Seong-Ho Guk and Professor Jeong-Chae Lee stated, "This study demonstrated that fine particulate matter and Type 2 diabetes mellitus act synergistically to promote senescence and functional decline of bone marrow stem cells. In particular, by confirming that inhibition of the NLRP3 inflammasome can mitigate this damage, we have provided scientific evidence for the development of prevention and treatment strategies for chronic disease patients vulnerable to environmental pollution."

Meanwhile, PhD candidate 리잘성커르 (Department of Bioactive Material Sciences) and Dr. 고빈다 (School of Dentistry) participated as co-first authors, and the study was carried out with support from the Ministry of Science and ICT's Core Leap Research Support Program.