GATA3 Macrophages as a Contributing Cause of Cardiac Fibrosis

The innate immune cells called macrophages are deeply involved in both inflammation and regeneration. They adopt different phenotypes, or polarizations, depending on circumstances, such as the M1 polarization (inflammatory, aggressive in pursuit of pathogens) and M2 polarization (pro-regenerative, anti-inflammatory). The simple view of macrophage polarization in aging tissues is that problems arise with an excess of M1 macrophages, and this is a part of the chronic inflammation that is characteristic of aging. It is well known that inflammation, when maintained over the long term, is highly disruptive of tissue function, and contributes to the progression of all of the common age-related disease. The open access commentary here makes the point that this model of polarization and inflammation is overly simplistic, and the reality is much more complex. The researchers illustrate this with data on M2 macrophages expressing GATA3, suggesting that it is these cells, rather than pro-inflammatory M1 macrophages, that are contributing to the fibrosis that appears in cardiac tissue with age. Fibrosis is a disarray of tissue maintenance and regeneration, involving the deposition of scar-like collagen structures that degrade tissue function. The usual view of fibrosis is that it is a consequence of inflammation, very connected to the inflammatory presence of senescent cells, for example. Given that, it is quite interesting to see this sort of contradictory data. Chronic ...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs