Spatiotemporal signaling underlies progressive vascular rarefaction in myocardial infarction.
Lin Wei TungElena GroppaHesham SolimanBruce LinChihkai ChangChun Wai CheungMorten RitsoDavid GuoLucas RempelSarthak SinhaChristine EisnerJulyanne BrassardKelly M McNagnyJeff BiernaskieFabio M V RossiPublished in: Nature communications (2023)
Therapeutic angiogenesis represents a promising avenue to revascularize the ischemic heart. Its limited success is partly due to our poor understanding of the cardiac stroma, specifically mural cells, and their response to ischemic injury. Here, we combine single-cell and positional transcriptomics to assess the behavior of mural cells within the healing heart. In response to myocardial infarction, mural cells adopt an altered state closely associated with the infarct and retain a distinct lineage from fibroblasts. This response is concurrent with vascular rarefaction and reduced vascular coverage by mural cells. Positional transcriptomics reveals that the infarcted heart is governed by regional-dependent and temporally regulated programs. While the remote zone acts as an important source of pro-angiogenic signals, the infarct zone is accentuated by chronic activation of anti-angiogenic, pro-fibrotic, and inflammatory cues. Together, our work unveils the spatiotemporal programs underlying cardiac repair and establishes an association between vascular deterioration and mural cell dysfunction.
Keyphrases
- single cell
- induced apoptosis
- cell cycle arrest
- heart failure
- left ventricular
- oxidative stress
- rna seq
- public health
- multiple sclerosis
- atrial fibrillation
- stem cells
- cell death
- radiation therapy
- acute coronary syndrome
- high throughput
- anti inflammatory
- mesenchymal stem cells
- healthcare
- rectal cancer
- ischemia reperfusion injury
- brain injury
- health insurance
- cerebral ischemia
- subarachnoid hemorrhage