The article "The role of immune cells and inflammation in pulmonary hypertension: mechanisms and implications" by Zhao et al. (2024) explores the complex relationship between immune cells, inflammation, and pulmonary hypertension (PH). PH is characterized by increased pulmonary vascular resistance and arterial pressure, leading to severe right heart failure or even death if untreated. The authors highlight that the development and progression of PH are closely associated with vascular remodeling, where immune-inflammatory reactions produce factors that damage the endothelium and disrupt the balance between vasodilating and vasoconstrictive substances. Perivascular inflammation is linked to increased intima, media, and adventitia thickness, as well as elevated pulmonary artery pressure. The review discusses the role of various immune cells, including T cells, B cells, macrophages, and dendritic cells (DCs), in the pathophysiology of PH. It emphasizes that these cells play crucial roles in maintaining vascular homeostasis, regulating immune responses, and influencing vascular remodeling. For instance, regulatory T cells (Tregs) help control other T cells and modulate monocytes, macrophages, DCs, natural killer cells, and B cells, thereby maintaining a balance between immunity and tolerance. However, disruptions in this balance can lead to chronic inflammation or autoimmune disorders. The article also examines the impact of cytokines and chemokines on PH. Cytokines such as IL-1β, IL-6, IL-10, IL-18, and TNF-α are found to be elevated in PH patients and animal models, contributing to vascular remodeling and disease progression. For example, IL-1β increases the production of prostacyclin (PGI2) and activates other cytokines, while IL-6 promotes excessive proliferation of pulmonary artery endothelial cells (PAECs) and smooth muscle cells (SMCs). Chemokines like CCL2, CCL5, and CX3CL1 are involved in monocyte and macrophage recruitment, leading to vascular remodeling and increased pulmonary artery pressure. Additionally, the article explores the role of vascular cells and the bone morphogenetic protein type 2 receptor (BMPR2) in immune regulation. BMPR2 mutations are identified as a primary genetic cause of PH, and its disruption leads to increased inflammation and impaired immune resolution. The authors suggest that targeting specific cytokine responses and pathways may be a promising therapeutic strategy for PH. Finally, the article reviews immunosuppressive therapies, including calcineurin inhibitors like tacrolimus and anti-CD20 monoclonal antibodies like rituximab, which have shown potential in reducing or reversing PH in animal models. However, the authors note that no immunosuppressants have been approved for PH treatment yet, and most immunomodulators are still in clinical trials. In conclusion, the article underscores the significant role of immune cells and inflammation in the pathophysiology of PH, highlightingThe article "The role of immune cells and inflammation in pulmonary hypertension: mechanisms and implications" by Zhao et al. (2024) explores the complex relationship between immune cells, inflammation, and pulmonary hypertension (PH). PH is characterized by increased pulmonary vascular resistance and arterial pressure, leading to severe right heart failure or even death if untreated. The authors highlight that the development and progression of PH are closely associated with vascular remodeling, where immune-inflammatory reactions produce factors that damage the endothelium and disrupt the balance between vasodilating and vasoconstrictive substances. Perivascular inflammation is linked to increased intima, media, and adventitia thickness, as well as elevated pulmonary artery pressure. The review discusses the role of various immune cells, including T cells, B cells, macrophages, and dendritic cells (DCs), in the pathophysiology of PH. It emphasizes that these cells play crucial roles in maintaining vascular homeostasis, regulating immune responses, and influencing vascular remodeling. For instance, regulatory T cells (Tregs) help control other T cells and modulate monocytes, macrophages, DCs, natural killer cells, and B cells, thereby maintaining a balance between immunity and tolerance. However, disruptions in this balance can lead to chronic inflammation or autoimmune disorders. The article also examines the impact of cytokines and chemokines on PH. Cytokines such as IL-1β, IL-6, IL-10, IL-18, and TNF-α are found to be elevated in PH patients and animal models, contributing to vascular remodeling and disease progression. For example, IL-1β increases the production of prostacyclin (PGI2) and activates other cytokines, while IL-6 promotes excessive proliferation of pulmonary artery endothelial cells (PAECs) and smooth muscle cells (SMCs). Chemokines like CCL2, CCL5, and CX3CL1 are involved in monocyte and macrophage recruitment, leading to vascular remodeling and increased pulmonary artery pressure. Additionally, the article explores the role of vascular cells and the bone morphogenetic protein type 2 receptor (BMPR2) in immune regulation. BMPR2 mutations are identified as a primary genetic cause of PH, and its disruption leads to increased inflammation and impaired immune resolution. The authors suggest that targeting specific cytokine responses and pathways may be a promising therapeutic strategy for PH. Finally, the article reviews immunosuppressive therapies, including calcineurin inhibitors like tacrolimus and anti-CD20 monoclonal antibodies like rituximab, which have shown potential in reducing or reversing PH in animal models. However, the authors note that no immunosuppressants have been approved for PH treatment yet, and most immunomodulators are still in clinical trials. In conclusion, the article underscores the significant role of immune cells and inflammation in the pathophysiology of PH, highlighting