Do bone marrow mononuclear cell-derived macrophages ameliorate adverse cardiac remodeling in a mouse model of transverse aortic constriction?
BMNC-derived macrophages ameliorate adverse cardiac remodeling and preserve LV function in a mouse model of pressure overload, suggesting a potential novel therapeutic pathway for heart failure.
Introduction: Heart failure (HF) caused by pressure overload remains as one of the leading causes of morbidity and mortality worldwide, which can manifest itself in a wide range of clinical scenarios. Current therapeutic strategies are limited to lifestyle changes, pharmacological measures, and devices aimed at supporting heart function. This poses a challenge in the search for new strategies for disease management. Macrophages, constituting nearly 10 % of non-myocyte cells in a healthy heart are considered a means to fill this gap due to their pleiotropic phenotype, which extends beyond the well-known functions of phagocytosis and antigen presentation. In this study, we evaluated the efficacy of bone marrow mononuclear cell (BMNC)-derived macrophages (BMNC-Mφ) in treating a mouse model of transverse aortic constriction (TAC). Methods: transcriptome dynamics over time using time-resolved deep RNA sequencing profiles of heart tissues from healthy, 1 day post-TAC, 8 days post-TAC, and 16 days post-TAC mice. Time-course transcriptomic profiling was followed by histological analysis of excised hearts on day 28. Results: , p < 0.05) and controlled cardiomyocyte growth, which was seen in the smaller short-axis diameter of cardiomyocytes in BMNC-Mφ-treated group (17.2 ± 0.18 μm vs. 19.45 ± 0.46 μm, p < 0.05). Conclusion: The main conclusion drawn from our results is that BMNC-Mφ improved or at least preserved LV function and architecture through metabolic recovery, immunosuppression, organized cell cycle/proliferation, and fibrosis modulation.
Yakhshimurodov et al. (Fri,) studied this question.