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Interleukin-1β (IL-1β) is a vital cytokine that plays an important role in regulating immune responses to infectious challenges and sterile insults. In addition, two endogenous inhibitors of functional receptor binding, IL-1 receptor antagonist (IL-1Ra), complete the family. To gain biological activity, IL-1β requires processing by the protease caspase-1 and activation of inflammasomes. Numerous clinical association studies and experimental approaches have implicated members of the IL-1 family, their receptors, or components of the processing machinery in the underlying processes of cardiovascular diseases. Here, we summarize the current state of knowledge regarding the pro-inflammatory and disease-modulating role of the IL-1 family in aneurysm. We discuss clinical evidence, signalling pathway, and mechanism of action and last, lend a perspective on currently developing therapeutic strategies involving IL-1β in aneurysm.

Aortic dissection and aortic aneurysms are currently among the most high-risk cardiovascular diseases due to their rapid onset and high mortality. Although aneurysm research has been extensive, the pathogenesis remains unknown. Studies have found that the TGF-β/Smad pathway and aneurysm formation appear linked. For example, the TGF-β signaling pathway was significantly activated in aneurysm development and aortic dissection. Aneurysms are not, however, mitigated following knockdown of TGF-β signaling pathway-related genes. Incidence and mortality rate of ruptured thoracic aneurysms increase with the down-regulation of the classical TGF-β signaling pathway. In this review, we summarize recent findings and evaluate the differential role of classical and non-classical TGF-β pathways on aortic aneurysm. It is postulated that the TGF-β signaling pathway is necessary to maintain vascular function, but over-activation will promote aneurysms whereas over-inhibition will lead to bypass pathway over-activation and promote aneurysm occurrence.

Objective(s): The stress-responsive genes of Sestrin family are recognized as new tumor suppressor genes in breast carcinoma, however, the function of Sestrin family in human prostate cancer is not clear. Ionizing radiation (IR) is known to induce Sestrin gene expression in breast cancer cells. However, the response of Sestrin to IR has not been reported in PC3 prostate cancer cells. Materials and Methods: Sestrin2 expression in prostate cancer cell lines (PC3, LNCaP clone FGC, and DU145) was detected by Western blot and real-time PCR. Cell counting kit (CCK-8) was used to detect cellular proliferation. The radiosensitivity of PC3 cells was detected by clonogenic assay. Results: Sestrin2 expression in prostate cancer cell lines (PC3, LNCaP clone FGC, and DU145) is low. In vitro assays indicated that over-expressing Sestrin2 in human prostate cancer PC3 inhibited tumor proliferation. In addition, elevated Sestrin2 expression sensitized PC3 cells to IR. Conclusion: We determined Sestrin2 may function as a tumor suppressor through repressing proliferation, mediating sensitization to IR in PC3 cells.