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TRAP1 Improves Diabetic Retinopathy by Preserving Mitochondrial Function.

Yuchen Li¹, Weida Xu¹, Guiyang Zhao¹

¹Department of Ophthalmology, Nanjing First Hospital, Nanjing Medical University, Nanjing, People's Republic of China.

Clinical Ophthalmology (Auckland, N.Z.)

|July 21, 2025

Summary

This summary is machine-generated.

Tumor necrosis factor-associated protein 1 (TRAP1) protects against diabetic retinopathy (DR) by maintaining mitochondrial function and reducing ferroptosis. Lower TRAP1 levels contribute to DR-related mitochondrial damage and cell death.

Keywords:

TRAP1 diabetic retinopathy ferroptosis mitochondria oxidative stress

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Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides

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Published on: September 16, 2020

Area of Science:

Ophthalmology
Cell Biology
Molecular Medicine

Background:

Mitochondrial dysfunction is a key factor in early diabetic retinopathy (DR).
Tumor necrosis factor-associated protein 1 (TRAP1), a mitochondrial chaperone, has not been studied in DR.
Investigating TRAP1's role is crucial for understanding DR pathogenesis.

Purpose of the Study:

To investigate the role of TRAP1 in diabetic retinopathy.
To determine TRAP1's effect on mitochondrial function and ferroptosis in retinal cells.
To explore TRAP1's potential as a therapeutic target for DR.

Main Methods:

Established in vivo and in vitro models of diabetic retinopathy.
Assessed TRAP1 expression using Western blotting, RT-qPCR, and immunofluorescence.
Evaluated cell viability, ROS, mitochondrial damage, and ferroptosis in ARPE-19 cells.
Utilized RNA sequencing and co-immunoprecipitation to identify interacting proteins.

Main Results:

TRAP1 expression was significantly reduced in diabetic rat retinas and high glucose-treated ARPE-19 cells.
Reduced TRAP1 impaired cell viability, increased ROS, and caused mitochondrial dysfunction.
TRAP1 overexpression protected mitochondrial homeostasis and enhanced cell viability.
TRAP1 mitigated hyperglycemia-induced mitochondrial damage by reducing ferroptosis.

Conclusions:

TRAP1 protects mitochondrial function in retinal cells.
Decreased TRAP1 levels are implicated in early diabetic retinopathy-induced mitochondrial dysfunction.
TRAP1's interaction with ferroptosis proteins enhances cellular resilience and viability.