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Deletion of soluble epoxide hydrolase suppressed chronic kidney disease-related vascular calcification by restoring

Wanbing He1, Jieping Huang1, Yang Liu2,3

  • 1Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107 Yanjiang Road, Guangzhou, 510120, China.

Cell Death & Disease
|October 24, 2021
PubMed

Insights

Soluble epoxide hydrolase (sEH) deletion prevents vascular calcification in chronic kidney disease (CKD) models. This inhibition occurs by preserving Sirtuin 3 (Sirt3) levels, protecting mitochondrial function and suppressing vascular smooth muscle cell calcification.

Area of Science:

  • Nephrology
  • Cardiovascular Biology
  • Biochemistry

Background:

  • Vascular calcification is a common complication of chronic kidney disease (CKD), significantly increasing cardiovascular disease (CVD) risk.
  • Current therapies for vascular calcification in CKD are limited, highlighting the need for novel therapeutic targets.

Purpose of the Study:

  • To investigate the role of soluble epoxide hydrolase (sEH) in mediating vascular calcification within the context of CKD.
  • To explore the potential of targeting sEH as a therapeutic strategy for preventing vascular calcification.

Main Methods:

  • Utilized knockout (Ephx2-/-) and wild-type (WT) mice fed a high adenine and phosphate (AP) diet to model CKD-induced vascular calcification.
  • Assessed vascular calcification, vascular smooth muscle cell (VSMC) phenotypic transition, and Sirtuin 3 (Sirt3) expression under high phosphorus (Pi) conditions.
  • Investigated the interaction between sEH and Sirt3 and its impact on mitochondrial function.

Main Results:

  • Deletion of sEH significantly inhibited AP-induced vascular calcification in mice.
  • sEH deficiency abolished high Pi-induced VSMC phenotypic transition, independent of epoxyeicosatrienoic acids (EETs) hydrolysis.
  • sEH interacted with and destabilized Sirt3 under high Pi, leading to Sirt3 degradation; sEH deletion preserved Sirt3, maintaining mitochondrial ATP synthesis and morphology, thereby suppressing VSMC calcification.

Conclusions:

  • Soluble epoxide hydrolase (sEH) plays a crucial role in promoting vascular calcification in CKD.
  • Inhibition of sEH preserves Sirt3 expression and mitochondrial function, effectively suppressing VSMC calcification.
  • Targeting sEH represents a promising therapeutic strategy for preventing vascular calcification in CKD patients.

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