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Recent publication of Hegyi and Sahin-Tóth reported that CPA1 p.n256K mutant mice developed chronic pancreatitis (CP) through endoplasmic reticulum stress.1 This, along with other animal models based on CP genetic variants, revealed that the clinical course and mechanism of CP are better recapitulated with in vivo methods.2
Previously, we found that SPINK1 c.194+2T>C mutation is the most frequently observed variant in Chinese patients with idiopathic CP. Function of c.194+2T>C variant has been characterised through in vitro studies as resulting in the absence of serine protease inhibitor secretion.3 4 However, the unavailability of SPINK1 c.194+2T>C animal model hindered the study into its role in CP development. To date, the only in vivo study focused on phenotype of homozygous Spink1 (also known as Spink3) deleted mice and found that they died of autophagic acinar cell death within 15 days after birth.5 Considering over 80% of Chinese CP patients with SPINK1 c.194+2T>C variant carry heterozygous mutation,6 we hypothesise that a heterozygous c.194+2T>C variant animal model may practically sketch the clinical pattern of …
CS, ML and WA contributed equally.
Contributors CS, ZL and ZSL designed and directed the study. CS, MYL and WA performed experiments and performed data analysis. HJ preformed histological analysis. CS, MYL and WA drafted the manuscript. All authors interpreted the data. XTM, WBZ and HW revised the manuscript. All authors approved the final manuscript.
Funding Support for this study came from the National Natural Science Foundation of China (grant numbers 81470885 (CS) and 81670585 (ZSL)), the Scientific Innovation Program of Shanghai Municipal Education Committee (ZL) and the Shuguang Program of Shanghai Education Development Foundation and Municipal Education Commission (grant number 15SG33 (ZL)).
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
Patient consent for publication Not required.
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