Key result
Novel lysine acylations link altered metabolism to gene regulation in cardiac hypertrophy and heart failure.
Why the study?
Research on novel lysine acylations associated with cardiac hypertrophy and heart failure has been steadily increasing, necessitating a summary of their roles and significance.
Novel non-histone and histone lysine acylations represent an emerging epigenetic and metabolic link in the pathogenesis of heart failure, offering new potential targets for therapeutic intervention.
Pathological cardiac hypertrophy is a primary contributor to heart failure (HF).Protein acylation, particularly acetylation, plays a crucial role in this process.Advances in mass spectrometry and proteomics have identified an increasing number of novel lysine acylation modifications, including crotonylation, lactylation, succinylation, βhydroxybutyrylation, 2-hydroxyisobutyrylation, propionylation and malonylation.These novel acylations are implicated in key physiological processes and disease-related cellular functions, as they modify the physicochemical properties of proteins and closely link substrate metabolism to gene regulation.Research on these novel lysine acylations associated with cardiac hypertrophy and HF has been steadily increasing in recent years.This review aims to summarize the progress and significance of these novel lysine acylations in cardiac hypertrophy and HF, providing references for a deeper understanding of the pathogenesis of HF and development of innovative therapeutic strategies.
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Kang et al. (2026) conducted a review in Heart failure and pathological cardiac hypertrophy. Novel lysine acylation modifications was evaluated. Novel lysine acylations link substrate metabolism to gene regulation and play key roles in the pathogenesis of pathological cardiac hypertrophy and heart failure.
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