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Cell damage (also known as cell injury) is a variety of changes of stress that a cell suffers due to external as well as internal environmental changes. Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors. Cell damage can be reversible or irreversible.
HMGB1 can also induce dendritic cell maturation via upregulation of CD80, CD83, CD86 and CD11c, and the production of other pro-inflammatory cytokines in myeloid cells (IL-1, TNF-a, IL-6, IL-8), and it can lead to increased expression of cell adhesion molecules (ICAM-1, VCAM-1) on endothelial cells.
Phagocytosis of an otherwise-viable cell may occur because the cell is recognised as stressed, activated, senescent, damaged, pathogenic or non-self, or is misrecognised. Cells are phagocytosed as a result of: i) expressing eat-me signals on their surface, ii) losing don’t-eat-me signals, and/or iii) binding of opsonins. It is clear that ...
Necrosis is cell death where a cell has been badly damaged through external forces such as trauma or infection and occurs in several different forms. It is the sum of what happens to cells after their deaths. [20] In necrosis, a cell undergoes swelling, followed by uncontrolled rupture of the cell membrane with cell contents being expelled.
Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytes are able to engulf and remove before the contents of the cell can spill out onto surrounding cells and cause damage to them. [5] Because apoptosis cannot stop once it has begun, it is a highly regulated process.
Red blood cells are also removed from the damaged tissue by macrophages. 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 ...
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR.
High levels of intracellular Ca 2+, the major cause of post-injury cell damage, [30] destroy mitochondria, [11] and trigger phospholipases and proteolytic enzymes that damage Na+ channels and degrade or alter the cytoskeleton and the axoplasm. [31] [26] Excess Ca 2+ can also lead to damage to the blood–brain barrier and swelling of the brain ...