Proteomics

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Mitochondrial protein lactylation in myocardial infarction

ABSTRACT: Lactylation, a novel post-translational modification (PTM), in which a lactyl group, derived from lactate, is covalently added to lysine residues on the target proteins. Lactylation, first observed in histones in 2019, is increasingly recognized for its influence on gene expression, especially as it relates to shifts in cellular metabolism. ‘Metabolic reprogramming’ is one of the hallmarks of the myocardial infarction (MI), where cardiomyocytes shift from fatty acid oxidation to anaerobic glycolysis to meet energy demands, producing lactate. Very few studies suggest a positive correlation between increased lactate levels and mortality in heart failure patients, implying the importance of lactylation in the pathogenesis of MI. However, knowledge of lactylation post-MI is currently limited. The project aims to understand the differences in mitochondrial lactylated proteins and their relevance in the progression or restoration of MI pathogenesis. We also utilize AZD3965, a selective inhibitor of monocarboxylate transporter 1, which is responsible for bidirectional transport of lactate, to understand the lactylation profiling in MI.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Hadi Pourhadi  

LAB HEAD: Dhanendra Tomar

PROVIDER: PXD068087 | Pride | 2026-06-08

REPOSITORIES: pride

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20250702_Tomar_Shani_Magneticbeads_mouse_heart_01.raw Raw
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Publications

Metabolic reprogramming is a hallmark of myocardial infarction (MI), in which cardiomyocytes shift from fatty acid oxidation to anaerobic glycolysis, leading to elevated lactate production and mitochondrial dysfunction. Lactylation, a recently discovered lysine post-translational modification, has emerged as a metabolic signaling mechanism; however, its role within mitochondria during MI remains poorly understood. Here, we mapped the mitochondrial lactylome following MI and examine how modulatio  ...[more]

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