Pulmonary fibrosis is a chronic, diffuse, interstitial lung disease involving the pulmonary interstitium, alveoli, and bronchioles caused by various causes. There is no effective treatment. Currently, exogenous bone marrow-derived mesenchymal stem cells (BM-MSCs) transplantation has attracted much attention as a new stem cell therapy in the treatment of pulmonary fibrosis. Less attention has been paid to the functional status of endogenous BM-MSCs during pulmonary fibrosis. Based on summary on the anti-pulmonary fibrosis effect of BM-MSCs and its mechanism, this review further discusses the abnormal changes of bone marrow function in animals with pulmonary fibrosis and the role of glutamate NMDA receptor overactivation in mediating the functional inhibition of endogenous BM-MSCs induced by pulmonary fibrosis. This will provide potential ideas for finding effective treatments for pulmonary fibrosis.
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