Key result
Depletion of Cd34+ cells alleviated the severity of ventricular fibrosis and improved cardiac function after ischemia/reperfusion injury.
Why the study?
Ambiguous results from multiple CD34+ cell-based therapeutic trials in heart disease have halted large-scale stem/progenitor cell application, leaving the biological functions of heterogeneous CD34+ cell populations and their net effect on cardiac remodeling unclear.
Population
Human and mouse ischemic hearts, including an inducible Cd34 lineage-tracing mouse model
Comparison
Depletion of Cd34+ cells vs non-depletion after ischemia/reperfusion injury
Design
Preclinical animal and translational human tissue study using single-cell RNA sequencing and lineage tracing
Authors
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Cd34+ depletion attenuates post-I/R fibrosis in animals; hypothesis-generating for human remodeling therapies, should not yet change practice.
Heterogeneous CD34+ cell populations actively participate in post-infarction cardiac remodeling by differentiating into profibrotic mesenchymal cells, angiogenic endothelial cells, and pro-inflammatory macrophages.
Xie et al. (2023) studied Myocardial ischemia/reperfusion injury. Depletion of Cd34+ cells vs. Control mice was evaluated on Severity of ventricular fibrosis and cardiac function after ischemia/reperfusion injury. Depletion of Cd34+ cells alleviated the severity of ventricular fibrosis and improved cardiac function after ischemia/reperfusion injury.
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