An hematopoietic-vascular niche regulates alveolar repair and lung fibrosis
Tissue repair is a finely tuned process involving a complex balance between regeneration and scarring. This balance is influenced among other parameters by the extent of the lesion, and the regenerative potential of the injured organ.
Lung and liver are organs with tremendous regenerative potential when compared to others like the heart, and the brain, notorious for their poor regenerative capacities.
However, years of chronic exposure to noxious agents such as cigarette smoke, and alcohol, can lead to the exhaustion of their regenerative capabilities, the accumulation of scar tissue, and ultimately to their failure.
Using an improved model of Idiopathic Pulmonary Fibrosis (IPF), based on repetitive intratracheal administrations of bleomycin in mice, Cao Z et al., have shown the central role played by the interaction between macrophages and microvascular endothelial cells in directing lung repair toward regeneration or scarring.
In the long-term, these results might lead to the development of drugs aiming at preventing fibrosis by supporting lung regeneration.
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