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Macrophages repair wounds and remodel tissue by producing extracellular matrix and proteases to modify that specific matrix. [1] A myocardial infarction induces tissue remodeling of the heart in a three-phase process: inflammation, proliferation, and maturation. Inflammation is characterized by massive necrosis in the infarcted area ...
Timing is important to wound healing. Critically, the timing of wound re-epithelialization can decide the outcome of the healing. [11] If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months; [12] [13] If the epithelization of a wounded area is fast, the healing will result in regeneration.
Failure to remove all of the damaged cells and pathogens may retrigger inflammation. The two subsets of macrophage M1 & M2 plays a crucial role in this phase, M1 macrophage being a pro inflammatory while as M2 is a regenerative and the plasticity between the two subsets determine the tissue inflammation or repair. [citation needed]
Inflammation is a generic response, and therefore is considered a mechanism of innate immunity, whereas adaptive immunity is specific to each pathogen. [2] Inflammation is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out ...
In major injuries, the repair mechanisms are unable to restore the skin to its original condition. The repaired region contains an abnormally large number of collagenous fibers, and relatively few blood vessels. Damaged sweat and sebaceous glands, hair follicles, muscle cells, and nerves are seldom repaired.
Inflammaging is thought to be caused by a loss of control over systemic inflammation resulting in chronic overstimulation of the innate immune system. Inflammaging is a significant risk factor in mortality and morbidity in aged individuals. [2] [3] [4] Inflammation is essential to protect against viral and bacterial infection, as well as ...
Macrophage polarization is a process by which macrophages adopt different functional programs in response to the signals from their microenvironment. This ability is connected to their multiple roles in the organism: they are powerful effector cells of the innate immune system, but also important in removal of cellular debris, embryonic development and tissue repair.
The inflammasome was discovered by the team of Jürg Tschopp, at the University of Lausanne, in 2002. [17] [18] In 2002, it was first reported by Martinon et al. [17] that NLRP1 (NLR family PYD-containing 1) could assemble and oligomerize into a structure in vitro, which activated the caspase-1 cascade, thereby leading to the production of pro-inflammatory cytokines, including IL-1β and IL-18.