Insights on post-translational modifications in fatty liver and fibrosis progression

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2025, Номер 1871(3), С. 167659 - 167659

Опубликована: Янв. 7, 2025

Язык: Английский

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Functional mechanisms and potential therapeutic strategies for lactylation in liver disease

Life Sciences, Год журнала: 2025, Номер 363, С. 123395 - 123395

Опубликована: Янв. 13, 2025

Язык: Английский

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SOX9: a key transcriptional regulator in organ fibrosis

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Фев. 5, 2025

The SOX9 gene locus is not only extensive but also intricate, and it could promote fibrosis in different organs or tissues, including cardiac fibrosis, liver kidney pulmonary as well other organ fibrosis. Many disorders are associated with the process of fibrosis; moreover, a common symptom chronic inflammatory diseases, characterized by accumulation excessive components extracellular matrix through signaling pathways. advanced stage fibrotic leads to dysfunction and, ultimately, death. In this review, we first give an overview original structure functions SOX9. Second, will discuss role various tissues. Third, describe reveal possibility antifibrotic treatment target. Finally, focus on application novel technologies for subsequent investigation

Язык: Английский

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Detecting the distribution patterns of histone lactylation in the mouse testis at different developmental stages

Gene, Год журнала: 2025, Номер unknown, С. 149355 - 149355

Опубликована: Фев. 1, 2025

Язык: Английский

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Mechanisms for Regulatory Effects of Exercise on Metabolic Diseases from the Lactate–Lactylation Perspective

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(8), С. 3469 - 3469

Опубликована: Апрель 8, 2025

Metabolic diseases, including cardiovascular type 2 diabetes mellitus (T2DM), osteoporosis, and non-alcoholic fatty liver disease (NAFLD), constitute a major global health burden associated with chronic morbidity mortality. Lactate, once considered as metabolic byproduct, has emerged key regulator of cellular reprogramming through lactylation, novel post-translational modification (PTM) that dynamically couples flux to chromatin remodeling. Lactylation exerts dual regulatory roles signaling molecule via GPR81/GPR4-mediated pathways substrate for the covalent histones enzymes. Pathologically, hyperlactatemia suppresses mitochondrial biogenesis, driving cardiomyopathy epigenetic silencing oxidative metabolism genes. Conversely, exercise-induced lactate surges transiently enhance insulin sensitivity AMPK/PGC-1α/GLUT4 signaling, resolve inflammation GPR81-mediated M2 macrophage polarization, restore function lactylation-dependent pathways. This review delineates lactylation spatiotemporal rheostat: dysregulation perpetuates disorders, whereas acute exercise-mediated remodels transcriptional networks homeostasis. Future research should integrate multiomics clarify lactylation’s dynamics, tissue-specific thresholds, metabolism–immunity interactions, metabolic–epigenetic crosstalk precision management diseases.

Язык: Английский

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Lactylation Modification in Cardio-cerebral Diseases: A State-of-the-art Review

Ageing Research Reviews, Год журнала: 2024, Номер unknown, С. 102631 - 102631

Опубликована: Дек. 1, 2024

Язык: Английский

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