Lymphangiogenic therapy VEGFCc156s improved angiotensin-II-induced impairments in heart function via novel mechanisms, which include transcriptional responses to alleviate inflammation and cardiac fibrosis, and systemic responses to ameliorate hypertension.
Mitochondrial-targeted SS-31 peptide ameliorates mitochondrial dysfunction and rescues pre-existing cardiac dysfunction in old mice, supporting the translational potential of mitochondrial protective interventions to treat age-related diseases.
Transgenic mice and cell models provide evidence of a pathophysiological mechanism that connects mtDNA damage to cardiac dysfunction via reduced NAD+ levels and loss of mitochondrial function and communication.
Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.
Cardiomyocyte Nox4 is a crucial physiological mediator of Nrf2 activation during acute exercise, triggering an adaptive response that preserves redox balance, mitochondrial and cardiac function to support normal physical exercise.