Overview

• Researchers have uncovered GADD45A as a critical factor in controlling the progression from adaptive to pathological cardiac hypertrophy, a precursor to heart failure.
• Mice lacking GADD45A exhibited severe cardiac fibrosis, inflammation, and hypertrophy, leading to significant structural and functional heart impairments.
• Overexpression of GADD45A in human cardiomyocytes mitigated inflammatory and fibrotic responses induced by TNF-α, underscoring its protective role.
• The study emphasizes the potential of GADD45A modulation as a therapeutic approach, particularly for type 2 diabetes patients at high risk of heart failure.
• GADD45A's broader functions in DNA repair, metabolic regulation, and oxidative stress protection further highlight its importance as a target for cardiovascular and metabolic diseases.