Impaired peroxisomal import in Drosophila oenocytes causes cardiac dysfunction by inducing upd3 as a peroxikine

Kerui Huang, Ting Miao, Kai Chang, Jinoh Kim, Ping Kang, Qiuhan Jiang, Andrew J. Simmonds, Francesca Di Cara and Hua Bai ()
Additional contact information
Kerui Huang: Iowa State University
Ting Miao: Iowa State University
Kai Chang: Iowa State University
Jinoh Kim: Iowa State University
Ping Kang: Iowa State University
Qiuhan Jiang: Iowa State University
Andrew J. Simmonds: University of Alberta
Francesca Di Cara: Dalhousie University
Hua Bai: Iowa State University

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract Aging is characterized by a chronic, low-grade inflammation, which is a major risk factor for cardiovascular diseases. It remains poorly understood whether pro-inflammatory factors released from non-cardiac tissues contribute to the non-autonomous regulation of age-related cardiac dysfunction. Here, we report that age-dependent induction of cytokine unpaired 3 (upd3) in Drosophila oenocytes (hepatocyte-like cells) is the primary non-autonomous mechanism for cardiac aging. We show that upd3 is significantly up-regulated in aged oenocytes. Oenocyte-specific knockdown of upd3 is sufficient to block aging-induced cardiac arrhythmia. We further show that the age-dependent induction of upd3 is triggered by impaired peroxisomal import and elevated JNK signaling in aged oenocytes. We term hormonal factors induced by peroxisome dysfunction as peroxikines. Intriguingly, oenocyte-specific overexpression of Pex5, the key peroxisomal import receptor, blocks age-related upd3 induction and alleviates cardiac arrhythmicity. Thus, our studies identify an important role of hepatocyte-specific peroxisomal import in mediating non-autonomous regulation of cardiac aging.

Date: 2020
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DOI: 10.1038/s41467-020-16781-w

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