Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Necrosis
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
===Other clinical classifications of necrosis=== # There are also very specific forms of necrosis such as [[gangrene]] (term used in clinical practices for limbs which have had severe hypoxia), [[gummatous]] necrosis (due to [[spirochaete|spirochaetal]] infections) and hemorrhagic necrosis (due to the blockage of venous drainage of an organ or tissue).{{citation needed|date=May 2023}} # Myonecrosis is the death of individual muscle fibres due to injury, hypoxia, or infection. Common causes include spontaneous diabetic myonecrosis (a.k.a. diabetic muscle infarction) and clostridial myonecrosis (a.k.a. [[gas gangrene]]).<ref>{{Cite web |title=Medical Definition of Myonecrosis; Doctor Written |url=https://www.rxlist.com/myonecrosis/definition.htm |access-date=2023-06-09 |website=RxList |language=en}}</ref> # Some [[spider bite]]s may lead to necrosis. In the United States, only spider bites from the [[brown recluse spider]] (genus [[Loxosceles]]) reliably progress to necrosis. In other countries, spiders of the same genus, such as the [[Chilean recluse]] in South America, are also known to cause necrosis. Claims that [[yellow sac spider]]s and [[hobo spider]]s possess necrotic [[venom]] have not been substantiated.{{citation needed|date=May 2023}} # In blind mole rats (genus ''[[Spalax]]''), the process of necrosis replaces the role of the systematic [[apoptosis]] normally used in many organisms. Low oxygen conditions, such as those common in blind mole rats' burrows, usually cause cells to undergo apoptosis. In adaptation to higher tendency of cell death, blind mole rats evolved a mutation in the [[tumor suppressor]] protein [[p53]] (which is also used in humans) to prevent cells from undergoing apoptosis. Human cancer patients have similar mutations, and blind mole rats were thought to be more susceptible to cancer because their cells cannot undergo apoptosis. However, after a specific amount of time (within 3 days according to a study conducted at the University of Rochester), the cells in blind mole rats release [[interferon-beta]] (which the immune system normally uses to counter viruses) in response to over-proliferation of cells caused by the suppression of apoptosis. In this case, the interferon-beta triggers cells to undergo necrosis, and this mechanism also kills cancer cells in blind mole rats. Because of tumor suppression mechanisms such as this, blind mole rats and other [[spalacid]]s are resistant to cancer.<ref>{{cite web| vauthors = Saey TH |title=Cancer cells self-destruct in blind mole rats|url=http://www.sciencenews.org/view/generic/id/346267/description/Cancer_cells_self-destruct_in_blind_mole_rats|website=[[Science News]]|publisher=[[Society for Science and the Public]]|access-date=27 November 2012|date=5 November 2012|archive-date=19 June 2013|archive-url=https://web.archive.org/web/20130619171046/http://www.sciencenews.org/view/generic/id/346267/description/Cancer_cells_self-destruct_in_blind_mole_rats|url-status=live}}</ref><ref name="pmid23129611">{{cite journal | vauthors = Gorbunova V, Hine C, Tian X, Ablaeva J, Gudkov AV, Nevo E, Seluanov A | title = Cancer resistance in the blind mole rat is mediated by concerted necrotic cell death mechanism | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 47 | pages = 19392β6 | date = November 2012 | pmid = 23129611 | pmc = 3511137 | doi = 10.1073/pnas.1217211109 | doi-access = free | bibcode = 2012PNAS..10919392G }}</ref>
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)