Metabolic remodeling during macrophage polarization in the context of myocardial infarction

Barth Syndrome (BTHS) is a rare X-linked genetic disorder characterized by cardiomyopathy, skeletal muscle weakness, growth delay, and altered lipid metabolism. The underlying molecular defects in the Tafazzin gene result in impaired cardiolipin synthesis, leading to mitochondrial dysfunction and compromised cellular energy production. Here, we aim to investigate the complex interplay between BTHS, macrophage polarization, and the immune response, with a specific focus on the role of Zymosan and LPS in modulating macrophage function. As key players in innate immunity, Macrophages undergo polarization into distinct phenotypes, namely M1 and M2, depending on the microenvironmental cues. M1 macrophages are associated with pro-inflammatory responses, while M2 macrophages are involved in tissue repair and immunoregulation. By employing wt and transgenic mice (TAZ knockdown) samples, we aim to elucidate the alterations in macrophage polarization patterns in the context of BTHS. Furthermore, the role of Zymosan, a potent immune stimulant, will be explored to understand its influence on macrophage polarization and subsequent immune responses in BTHS. The molecular mechanisms underlying these interactions will be investigated, focusing on signaling pathways, cytokine profiles, and lipid metabolism.