Progression of hepatic fibrosis requires sustained inflammation leading to activation of stellate cells into a fibrogenic and proliferative cell type, whereas regression is associated with stellate cell apoptosis. The contribution of hepatic macrophages to these events has been largely overlooked. However, a study in this issue of the JCI demonstrates that macrophages play pivotal but divergent roles, favoring ECM accumulation during ongoing injury but enhancing matrix degradation during recovery. These findings underscore the potential importance of hepatic macrophages in regulating both stellate cell biology and ECM degradation during regression of hepatic fibrosis.
Scott L. Friedman
Usage data is cumulative from August 2018 through August 2019.
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.