Publications by authors named "T Vico"
Background And Aims: Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a crucial role in cholesterol homeostasis by regulating low-density lipoprotein (LDL) receptor levels. Despite its known effects on cholesterol metabolism, the role of PCSK9 in cardiac function, especially post-myocardial infarction (MI), remains unclear. This study investigates the impact of PCSK9 on heart function post-MI and evaluates the effects of PCSK9 inhibition via Alirocumab.
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- Viral myocarditis involves the immune response to virus invasion, but the role of the GPR15 receptor in heart disease remains unclear.
- Researchers found that mice lacking GPR15 had trouble eliminating coxsackievirus B3, which resulted in harmful heart changes and dysfunction.
- The study suggests that GPR15 is crucial for the timely recruitment of regulatory T cells, and its absence leads to a prolonged inflammatory response and worse cardiac outcomes.
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- Clonal hematopoiesis of indeterminate potential (CHIP) is linked to increased risks for leukemia and cardiovascular diseases due to the presence of mutated myeloid cells; however, their specific behavior in cardiovascular tissues is not fully understood.
- The study involved patients undergoing cardiovascular surgeries, where researchers analyzed blood and tissue samples to identify CHIP mutation carriers and assess the characteristics of myeloid and lymphoid cells using advanced genetic techniques.
- Results showed that although CHIP-mutated myeloid cells did not accumulate more in cardiovascular tissues compared to non-mutated cells, they exhibited a more proinflammatory and disease-prone gene profile.
Middle-age abolishes cardioprotection conferred by thioredoxin-1 in mice.
Arch Biochem Biophys
March 2024
Thioredoxin-1 (Trx1) has cardioprotective effects on ischemia/reperfusion (I/R) injury, although its role in ischemic postconditioning (PostC) in middle-aged mice is not understood. This study aimed to evaluate if combining two cardioprotective strategies, such as Trx1 overexpression and PostC, could exert a synergistic effect in reducing infarct size in middle-aged mice. Young or middle-aged wild-type mice (Wt), transgenic mice overexpressing Trx1, and dominant negative (DN-Trx1) mutant of Trx1 mice were used.
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