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Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re-+ perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia).
Depending on the extent of injury, the cellular response may be adaptive and where possible, homeostasis is restored. [1] Cell death occurs when the severity of the injury exceeds the cell's ability to repair itself. [2] Cell death is relative to both the length of exposure to a harmful stimulus and the severity of the damage caused. [1]
Cardiovascular diseases are the leading cause of death worldwide, and have increased proportionally from 25.8% of global deaths in 1990, to 31.5% of deaths in 2013. [44] This is true in all areas of the world except Africa. [44] [45] In addition, during a typical myocardial infarction or heart attack, an estimated one billion cardiac cells are ...
Adult neurogenesis is also a form of cellular regeneration. For example, hippocampal neuron renewal occurs in normal adult humans at an annual turnover rate of 1.75% of neurons. [104] Cardiac myocyte renewal has been found to occur in normal adult humans, [105] and at a higher rate in adults following acute heart injury such as infarction. [106]
This impairs necessary blood flow and cuts off circulating oxygen, which can lead to tissue death and permanent damage to the brain, heart, arteries, and kidneys. This may occur as a result of chronic or poorly controlled hypertension, illicit drug use, or as a complication of pregnancy. [3]
In terms of repair models in the cell cycle, HR is only possible during the S and G2 phases, while NHEJ can occur throughout whole process. [3] These repair pathways are all regulated by the overarching DNA damage response mechanism. [4] Besides HR and NHEJ, there are also other repair models which exists in cells.
Most damage can be repaired without triggering the damage response system, however more complex damage activates ATR and ATM, key protein kinases in the damage response system. [92] DNA damage inhibits M-CDKs which are a key component of progression into mitosis. In all eukaryotic cells, ATR and ATM are protein kinases that detect DNA damage.
It can initiate apoptosis (i.e., programmed cell death) if DNA damage proves to be irreparable. It is essential for the senescence response to short telomeres. p53 pathway: In a normal cell, p53 is inactivated by its negative regulator, mdm2. Upon DNA damage or other stresses, various pathways will lead to the dissociation of the p53 and mdm2 ...