Kidney Week

Abstract: SA-PO159

Heat Acclimation Attenuates Ferroptosis and Prevents Heat Stress-Induced AKI by Enhancing Mitophagy

Session Information

• AKI: Metabolism and Cell Death
  October 26, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 103 AKI: Mechanisms

Authors

• Song, Yongwei, Department of Rheumatology and Clinical Immunology, Daping Hospital, Army Military Medical University, Chongqing, China

Yongwei Song, MS

• Chen, Wenting, Department of Rheumatology and Clinical Immunology, Daping Hospital, Army Military Medical University, Chongqing, China

Wenting Chen, MS

• Ling, Wang, Department of Rheumatology and Clinical Immunology, Daping Hospital, Army Military Medical University, Chongqing, China

Wang Ling, MD

• Xuesen, Yang, Department of Tropical Medicine, Army Military Medical University, Chongqing, China

Yang Xuesen, DrPH

• Zi, Dai Huan, Department of Rheumatology and Clinical Immunology, Daping Hospital, Army Military Medical University, Chongqing, China

Dai Huan Zi, PhD

Background

Exposure to a intense heat stress environment can lead to acute kidney injury (AKI), while heat acclimation(HA) can prevents the kidney against ischemic injury induced by intense heat stress. However, the mechanism underlying of the nephroprotective effect of HA remains unclear.It has been reported that ferroptosis is involved in heat stress-induced AKI.But，It is still unclear whether heat acclimation can exert renal protective effects by reducing ferroptosis.Furthermore,Mitophagy may influence the development of AKI through regulating intracellular iron metabolism, but it has not been reported in heat stress-induced AKI.

Methods

C57BL / 6 mice were divided into control group (CON), heat acclimation group (HA), heat stroke group (HS), heat stroke + heat acclimation group (HS+HA), and heat stroke+heat acclimation+3-MA group (HS+HA+3-MA).Among them, the mice in the HS group were kept in a high-temperature environment to establish the HS model.The mice in the HS+HA group were kept in low-temperature environment for 30 days to establish the HA model, followed by inducing the HS model.Mice in the HS+HA+3-MA group were subjected to high heat stress after consecutive intraperitoneal injection of 3-MA (20 mg/kg/day) for the last 7 days of the constructed HA model.The levels of mitophagy and ferroptosis were assessed in each group of mice.

Results

In the HS group, there was a significant increase ferroptosis. Moreover, heat acclimation significantly enhanced mitophagy and alleviated HS-induced ferroptosis.In contrast, Inhibiting mitophagy exacerbated ferroptosis and reversed the renoprotective effect of the heat acclimation .

Conclusion

Heat acclimation may prevent heat stress-induced acute kidney injury by alleviating ferroptosis through enhanced mitophagy.

Heat acclimation can enhance mitophagy

Funding

• Clinical Revenue Support