Many of the inflammatory and reparative processes led by macrophages are commonly observed after injury in the different tissues discussed in this article.

Of specific interest is that low adiponectin levels in AT and plasma of the severely obese subjects seems not to be related to the changes (increase) in AT macrophage infiltration but may rather be the result of inhibitory effects of adipokines (TNF-α and IL-6) released from the macrophages resident in the AT (7). 8, 21 April 2018 | European Journal of Epidemiology, Vol. 1, 14 December 2015 | Exercise Science, Vol. It is possible that careful lineage tracing may enable detection of additional developmental diversity in monocyte/macrophage lineages.

Comparison of the gene expression profiles of cardiac macrophages 3 days after MI on P1 and on P14 showed that the genes expressed in P1 macrophages were enriched in the gene ontology terms ‘angiogenesis’, ‘inflammation’, and ‘oxidative stress response’. 1, 1 October 2016 | Journal of Applied Physiology, Vol. For instance, several models have shown that suppression of the initial accumulation of monocyte-derived macrophages impairs muscle regeneration and clearance of necrotic tissues (18, 28, 55, 57, 58). Lipopolysaccharide stimulation results in the translocation of HDAC6 and cortactin from the cytosol to the cell periphery, promotes the formation of filopodial protrusions, and enhances microtubule acetylation around the microtubule-organizing center, all of which are abrogated by HDAC6 deficiency. Moreover, AMPK-dependent activation of FAO induced by miR-33 inhibition is associated with up-regulation of M2 markers (105), while Ampka1 deletion suppresses up-regulation of M2 markers in response to IL-4 or IL-10 in bone marrow-derived macrophages. The CD3+ T-cell fraction increases to ~35% of total CD45+ leukocytes by day 5 post-injury (42). 7, 11 April 2007 | Diabetologia, Vol. Soon after injury, Ly6Chi monocytes/macrophages derived from circulating Ly6Chi inflammatory monocytes infiltrate the injured muscle area (Fig. While some of the mechanisms, including phagocytosis of dying cells, are commonly observed in different tissues, many signals, such as cytokines and growth factors, may be tissue- and/or injury-specific. Macrophages within injured muscle are derived from circulating Ly6Chi monocytes. Consequently, repair and regeneration processes are tightly linked to initial inflammatory processes. Inhibiting macrophage accumulation reduces angiogenesis (110, 111), demonstrating that macrophages contribute to the proper vascularization of regenerating muscle tissue. 8, No. 8, 27 January 2014 | Journal of Primary Care & Community Health, Vol. Immune cells, in particular, mediate processes extending from the initial inflammation to the healing and regeneration phases. Deletion of integrin-β3 (Itgb3) increases the CD206+ (M2-like) cell fraction among macrophages and enhances fibrosis after cardiotoxin-induced muscle injury (115). Activated SCs also generate progeny that restore the pool of quiescent SCs. 82, No. 9, No. Regeneration and repair after injury. 46, No. By contrast, macrophages may also produce matrix metalloproteinases (MMPs) and other degradative enzymes that affect ECM.

Saclier, M., Cuvellier, S., Magnan, M., Mounier, R. and Chazaud, B. Cheng, M., Nguyen, M. H., Fantuzzi, G. and Koh, T. J. Perdiguero, E., Sousa-Victor, P., Ruiz-Bonilla, V., et al. Acharyya, S., Sharma, S. M., Cheng, A. S., et al. 6, 22 June 2016 | American Journal of Lifestyle Medicine, Vol. 13, No. 2, 29 April 2019 | BMC Infectious Diseases, Vol. Though these results are indicative of the pro-regenerative function of IL-6, inhibition of IL-6 receptor signaling using an antibody accelerates skeletal muscle regeneration and suppresses fibrosis after cardiotoxin injury (77). ECM synthesis and remodeling are also essential for formation of the scaffolding that supports regeneration.