VSMCs exhibit the remarkable plasticity required for development and adaptation of the cardiovascular system. The capacity of VSMCs to modulate their phenotype has evolved to facilitate angiogenesis and wound healing, but it has also been implicated in the pathogenesis of atherosclerosis, restenosis, posttransplant arteriopathy, and pulmonary hypertension. In this issue of the JCI, Boettger and colleagues report that the recently discovered Mir143/145 gene cluster promotes acquisition of the contractile phenotype of murine VSMCs (see the related article beginning on page 2634). These VSMC-restricted microRNAs, which target unique combinations of SMC genes, provide an efficient mechanism to fine-tune cardiovascular homeostasis and the response of the vessel wall to injury. This important discovery will open the door to new avenues of investigation and potentially future therapies for vascular diseases.
Michael S. Parmacek
Usage data is cumulative from August 2023 through August 2024.
Usage | JCI | PMC |
---|---|---|
Text version | 176 | 36 |
90 | 13 | |
Citation downloads | 30 | 0 |
Totals | 296 | 49 |
Total Views | 345 |
Usage information is collected from two different sources: this site (JCI) and Pubmed Central (PMC). JCI information (compiled daily) shows human readership based on methods we employ to screen out robotic usage. PMC information (aggregated monthly) is also similarly screened of robotic usage.
Various methods are used to distinguish robotic usage. For example, Google automatically scans articles to add to its search index and identifies itself as robotic; other services might not clearly identify themselves as robotic, or they are new or unknown as robotic. Because this activity can be misinterpreted as human readership, data may be re-processed periodically to reflect an improved understanding of robotic activity. Because of these factors, readers should consider usage information illustrative but subject to change.