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We read with interest the recent paper by Zhao et al,1 which reported that stimulator of interferon genes (STING) signalling alleviated chronic pancreatitis (CP)-induced inflammation and fibrosis. There is increasing evidence that STING activation could lead to inflammatory response and fibrosis. In our opinion, this contention is associated with three major issues: the form of stimulators that activate STING, the degree of STING activation and the type of immune cell lineages activated STING signalling are able to affect its role in the process of disease.
Self-DNA released from various types of cells during infection or inflammation may stimulate cyclic guanosine monophosphate–adenosine monophosphate (GMP–AMP) synthase (cGAS)–STING pathway to different degrees. Zhao et al 1 did not investigate how STING signalling was activated; however, the amount, manner and rate of DNA release under different ways of cell deaths all played important roles in activating downstream pathways. Additionally, recent reports indicated that the extent of DNA oxidation is a key factor in promoting an enhanced inflammatory …
Contributors QH, XW, DAS and JR participated in the design of this study. JW performed the statistical analysis. HR and LG carried out the study and collected important background information. QH drafted the manuscript. YR, GG, ZH and GW carried out the concepts, design, definition of intellectual content, literature search and data analysis.
Funding This work was supported by National Natural Science Foundation of China (No. 81571881, No. 81772052 and No. 81801971).
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
Patient consent for publication Not required.
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