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Kidney Week

Abstract: PO2621

Grb2 Promotes Cardiorenal Syndrome Type 3: Roles of Cardiomyocyte Contractile Cytoskeleton, Mitochondria Damage, and Inflammation Response

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention


  • Wang, Jin, Chinese PLA General Hospital, Beijing, Beijing, China
  • Chen, Xiangmei, Chinese PLA General Hospital, Beijing, Beijing, China

Cardiorenal syndrome type-3 (CRS-3) is a damage to heart following acute kidney injury. Although many experiments have found that inflammation, oxidative stress, and cardiomyocyte death are involved in cardiomyocyte pathophysiological alterations during CRS-3, it lacks a non-bias analysis to figure out the primary mediator of cardiac dysfunction.Herein, the aim of our study is to figure out the primary upstream regulator of these intracellular molecular biological events.


In this study, proteomic analysis was operated in CRS-3 and growth factor receptor-bound protein 2 (Grb2) was identified as a regulator involving AKI-related myocardial damage.


Increased Grb2 was associated with cardiac diastolic dysfunction, mild cardiomyocyte death and prominent myocardial inflammation; these pathological changes could be reversed through administration of Grb2-blocking peptide after AKI. Molecular investigation illustrated that augmented Grb2 promoted cardiomyocytes contractile cytoskeleton degradation through inhibiting the expression of Myosin. In addition, increased Grb2 triggered mitochondrial fission, inactivated mitochondrial autophagy, induced mitochondrial potential reduction, and triggered caspase-9/3 activation. Pro-inflammatory signaling pathways, including NF-κB, MAPK/JNK, and MAPK/p38, were activated by Grb2 in cardiomyocytes following AKI.


Our results identify CRS-3 is caused by Grb2 upregulation which contributes to cardiac dysfunction, cardiomyocyte apoptosis and myocardial inflammation. This finding provides a potential target for the clinical treatment of patients with CRS-3.