Fig. 4: The Kla modifications of functional proteins in cardiovascular diseases.
From: Lysine lactylation in diseases: beyond histone lactylation
The Kla modifications of functional proteins also play significant roles in the progression of cardiovascular diseases. The Kla modification of MDH2 and P4HB in cardiomyocyte can promote the accumulation of mitoROS to induce its ferroptosis and mitophagy. The Kla-modified α-MHC can also induce heart failure via regulating cell skeleton depolymerization. The Kla modifications of MeCP2 and Snail1 can also exerts protective and harmful effects to cardiomyocyte through modulating transcription of specific genes. Furthermore, the Kla modification of SA3K in fibroblasts could facilitate the survival of neighboring cardiomyocytes.
