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Emodin alleviates CRS4-induced mitochondrial damage via activation of the PGC1α signaling

Xin Dong1,2,3, Ruijia Wen1,2,3, Yuanyuan Xiong1,2,3

  • 1The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, China.

Phytotherapy Research : PTR
|January 10, 2024
PubMed

Insights

Emodin, a natural compound, protects the heart in cardiorenal syndrome type 4 (CRS4) by reducing kidney damage and improving cardiac function. It works by activating PGC1α signaling, mitigating mitochondrial damage in chronic kidney disease (CKD).

Area of Science:

  • Nephrology
  • Cardiology
  • Mitochondrial Biology

Background:

  • Cardiorenal syndrome type 4 (CRS4) is a severe complication of chronic kidney disease (CKD), leading to significant cardiac dysfunction and mortality.
  • Understanding the mechanisms underlying CRS4 is crucial for developing effective therapeutic interventions.

Purpose of the Study:

  • To investigate the potential cardioprotective effects of emodin in a mouse model of CRS4.
  • To elucidate the molecular pathways, particularly PGC1α signaling, involved in emodin's protective action.

Main Methods:

  • In vivo studies utilized a 5/6 nephrectomy mouse model to simulate CRS4.
  • In vitro experiments involved HL-1 cells exposed to CKD mouse serum.
  • Comprehensive assessments included echocardiography, histological analysis, immunofluorescence, biochemical assays, flow cytometry, qPCR, and Western blotting.

Main Results:

  • Emodin demonstrated protective effects on both kidney function/structure and cardiac morphology/function in the CRS4 model.
  • Emodin suppressed reactive oxygen species production and mitochondrial oxidative damage while enhancing oxidative metabolism.
  • These benefits were linked to the restoration of PGC1α expression and its downstream targets, with PGC1α inhibition reversing the cardioprotective effects.

Conclusions:

  • Emodin confers cardioprotection against 5/6 nephrectomy-induced mitochondrial damage in CRS4 by activating PGC1α signaling.
  • These findings suggest emodin as a potential therapeutic agent for managing CRS4 patients.

Keywords:
PGC1αcardiorenal syndrome type 4emodinmitochondria

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