The Role of TGF-β in Radiation and Chemotherapy Induced Pulmonary Fibrosis: Inhibition of TGF-β as a Novel Therapeutic Strategy

Role of interleukins in the pathogenesis of pulmonary fibrosis

Cell Death Discovery ◽

10.1038/s41420-021-00437-9 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Yi Xin She ◽

Qing Yang Yu ◽

Xiao Xiao Tang

Keyword(s):

Pulmonary Fibrosis ◽

Therapeutic Strategy ◽

Future Directions ◽

Regulation Mechanisms ◽

Underlying Mechanisms ◽

Multiple Cells ◽

The Relationship

AbstractInterleukins, a group of cytokines participating in inflammation and immune response, are proved to be involved in the formation and development of pulmonary fibrosis. In this article, we reviewed the relationship between interleukins and pulmonary fibrosis from the clinical, animal, as well as cellular levels, and discussed the underlying mechanisms in vivo and in vitro. Despite the effects of interleukin-targeted treatment on experimental pulmonary fibrosis, clinical applications are lacking and unsatisfactory. We conclude that intervening in one type of interleukins with similar functions in IPF may not be enough to stop the development of fibrosis as it involves a complex network of regulation mechanisms. Intervening interleukins combined with other existing therapy or targeting interleukins affecting multiple cells/with different functions at the same time may be one of the future directions. Furthermore, the intervention time is critical as some interleukins play different roles at different stages. Further elucidation on these aspects would provide new perspectives on both the pathogenesis mechanism, as well as the therapeutic strategy and drug development.

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The Role of Vascular Cell Senescence in Atherosclerosis: Antisenescence as a Novel Therapeutic Strategy for Vascular Aging

Current Vascular Pharmacology ◽

10.2174/1570161043476393 ◽

2004 ◽

Vol 2 (2) ◽

pp. 141-148 ◽

Cited By ~ 34

Author(s):

Tohru Minamino ◽

Hideyuki Miyauchi ◽

Toshihiko Yoshida ◽

Kaoru Tateno ◽

Issei Komuro

Keyword(s):

Therapeutic Strategy ◽

Cell Senescence ◽

Vascular Aging ◽

Vascular Cell ◽

Novel Therapeutic ◽

Vascular Cell Senescence

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Effect of SSH1/SSH2 expression changes by shRNA in glioma cell lines on response to radiotherapy and cofilin-1 reactivation.

Journal of Clinical Oncology ◽

10.1200/jco.2019.37.15_suppl.e13505 ◽

2019 ◽

Vol 37 (15_suppl) ◽

pp. e13505-e13505

Author(s):

Hong Xiao

Keyword(s):

Protein Phosphatase ◽

Glioma Cell ◽

Therapeutic Strategy ◽

Glioma Cells ◽

Protein Phosphatase 1 ◽

Migration And Invasion ◽

Radiation Induced ◽

U373 Cells ◽

Novel Therapeutic

e13505 Background: Radiotherapy has become the most important treatment for malignant glioma following surgery. However, development of radioresistance in glioma cells limits therapeutic efficacy. The slingshot (SSH) family of phosphatases is a potent regulator of Cofilin-1 activation. Methods: We investigate the role of SSH1(slingshot protein phosphatase 1) and SSH2 in radioresistance via using shRNA to block SSH1/2 expression in U251 and U373 cells as well as established radioresistant U251 (RR-U251) and U373 (RR-U373) cells. Results: We found that both SSH1 and SSH2-shRNA efficiently sensitized glioma cells to radiation with a sensitization enhancement ratio (SER) of 1.01-1.73. In SSH1-silenced cells, the cell viability, migration, and invasion abilities following radiation were remarkably reduced and radiation induced cell apoptosis was markedly enhanced compared with control cells. While in SSH2-silenced cells, the alterations were not as significant. Furthermore, the result of Western-blot suggested that radiosensization of SSH1/SSH2 silencing was mediated by inhibiting reactivation of phosphorylated CFL-1. Conclusions: Our study demonstrated that SSH1 and SSH2 are valid radiosensitizing targets in not only normal glioma cells but radioresistant lines, suggesting a novel therapeutic strategy to improve the efficacy of radiotherapy in patients with glioma.

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