Knockdown of HCK promotes HREC cell viability and inner blood–retinal barrier integrity by regulating the AMPK signaling pathway

TL;DR

Reducing HCK improves retinal cell health and blood barrier integrity in diabetic retinopathy by affecting the AMPK pathway.

Contribution

Identifies HCK as a novel therapeutic target in diabetic retinopathy through its regulation of AMPK signaling.

Findings

HCK expression increases in retinal cells under high glucose conditions.

Knockdown of HCK improves cell viability and blood-retinal barrier integrity.

HCK depletion suppresses the AMPK signaling pathway in diabetic retinopathy.

Abstract

Diabetic retinopathy (DR), a major complication of diabetes causing blindness, is characterized by retinal damage due to capillary degeneration and vascular leakage. Current treatments are not fully effective, highlighting the need for searching new therapeutic targets. Hematopoietic cell kinase (HCK), a protein involved in various diseases, has been identified as a potential biomarker in DR, but its role in disease progression requires further investigation. Here we investigated the role of HCK in DR and its potential mechanism. We found the expression of HCK increased under the stimulation of high glucose (HG) in human retinal capillary endothelial cells (HRECs). Knockdown of HCK can improve HREC cell viability and the integrity of the internal blood–retinal barrier. HCK depletion suppressed the AMPK pathway in HG-induced HRECs. In summary, HCK may be a potential target for the treatment of DR, which provides a theoretical basis for the development of new treatment strategies.

Figures