Racism has significantly impacted communities of color for centuries. The year 2020 is a reminder that racism is an ongoing public health crisis. Healthcare institutions have an important role in dismantling racism because of their ability to implement innovative solutions that advance diversity, address social determinants of health, and promote health equity. Healthcare professionals have the unique opportunity to support patients by discussing patients’ experiences of bias and racism. Asking about discrimination, however, can be difficult because of the sensitive nature of the topic and lack of appropriate education. This review highlights the importance of addressing patients’ experiences of racism, utilizing the frameworks of trauma-informed care, structural competency, provider bias, and intersectionality. Furthermore, this review provides ways to engage in meaningful dialogue around discrimination and includes important patient-centric resources.

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Cardiac progenitor cells (CPCs) have been shown to promote cardiac regeneration and improve heart function. However, evidence suggests that their regenerative capacity may be limited in conditions of severe hypoxia. Elucidating the mechanisms involved in CPC protection against hypoxic stress is essential to maximize their cardioprotective and therapeutic potential. We investigated the effects of hypoxic stress on CPCs and found significant reduction in proliferation and impairment of vasculogenesis, which were associated with induction of quiescence, as indicated by accumulation of cells in the G0-phase of the cell cycle and growth recovery when cells were returned to normoxia. Induction of quiescence was associated with a decrease in the expression of c-Myc through mechanisms involving protein degradation and upregulation of p21. Inhibition of c-Myc mimicked the effects of severe hypoxia on CPC proliferation, also triggering quiescence. Surprisingly, these effects did not involve changes in p21 expression, indicating that other hypoxia-activated factors may induce p21 in CPCs. Our results suggest that hypoxic stress compromises CPC function by inducing quiescence in part through downregulation of c-Myc. In addition, we found that c-Myc is required to preserve CPC growth, suggesting that modulation of pathways downstream of it may re-activate CPC regenerative potential under ischemic conditions.