Matches in SemOpenAlex for { <https://semopenalex.org/work/W3183360408> ?p ?o ?g. }
- W3183360408 endingPage "119099" @default.
- W3183360408 startingPage "119099" @default.
- W3183360408 abstract "Cellular senescence generates a permanent cell cycle arrest, characterized by apoptosis resistance and a pro-inflammatory senescence-associated secretory phenotype (SASP). Physiologically, senescent cells promote tissue remodeling during development and after injury. However, when accumulated over a certain threshold as happens during aging or after cellular stress, senescent cells contribute to the functional decline of tissues, participating in the generation of several diseases. Cellular senescence is accompanied by increased mitochondrial metabolism. How mitochondrial function is regulated and what role it plays in senescent cell homeostasis is poorly understood. Mitochondria are functionally and physically coupled to the endoplasmic reticulum (ER), the major calcium (Ca 2+ ) storage organelle in mammalian cells, through special domains known as mitochondria-ER contacts (MERCs). In this domain, the release of Ca 2+ from the ER is mainly regulated by inositol 1,4,5-trisphosphate receptors (IP3Rs), a family of three Ca 2+ release channels activated by a ligand (IP3). IP3R-mediated Ca 2+ release is transferred to mitochondria through the mitochondrial Ca 2+ uniporter (MCU), where it modulates the activity of several enzymes and transporters impacting its bioenergetic and biosynthetic function. Here, we review the possible connection between ER to mitochondria Ca 2+ transfer and senescence. Understanding the pathways that contribute to senescence is essential to reveal new therapeutic targets that allow either delaying senescent cell accumulation or reduce senescent cell burden to alleviate multiple diseases. • The basic concepts of cellular senescence • The role of Ca 2+ transfer between the endoplasmic reticulum and mitochondria through the IP3R in cellular senescence • The relationship between mitochondria-ER contact sites (MERCs) and cellular senescence • The role of cellular senescence in age-related diseases as well as the drugs available to counter their effects" @default.
- W3183360408 created "2021-08-02" @default.
- W3183360408 creator A5005190727 @default.
- W3183360408 creator A5056992130 @default.
- W3183360408 creator A5066461009 @default.
- W3183360408 creator A5070826281 @default.
- W3183360408 creator A5084102487 @default.
- W3183360408 date "2021-10-01" @default.
- W3183360408 modified "2023-09-27" @default.
- W3183360408 title "Keeping zombies alive: The ER-mitochondria Ca2+ transfer in cellular senescence" @default.
- W3183360408 cites W1524549603 @default.
- W3183360408 cites W1536843121 @default.
- W3183360408 cites W1546551973 @default.
- W3183360408 cites W1560166557 @default.
- W3183360408 cites W1580746914 @default.
- W3183360408 cites W1702885827 @default.
- W3183360408 cites W1834059013 @default.
- W3183360408 cites W1879159820 @default.
- W3183360408 cites W1910950086 @default.
- W3183360408 cites W1918750526 @default.
- W3183360408 cites W1968789295 @default.
- W3183360408 cites W1970703181 @default.
- W3183360408 cites W1971794940 @default.
- W3183360408 cites W1973712371 @default.
- W3183360408 cites W1977362098 @default.
- W3183360408 cites W1977956545 @default.
- W3183360408 cites W1981775109 @default.
- W3183360408 cites W1982481909 @default.
- W3183360408 cites W1987142903 @default.
- W3183360408 cites W1989560849 @default.
- W3183360408 cites W1991055482 @default.
- W3183360408 cites W1993316285 @default.
- W3183360408 cites W1996113298 @default.
- W3183360408 cites W1996642371 @default.
- W3183360408 cites W1997142695 @default.
- W3183360408 cites W2003346248 @default.
- W3183360408 cites W2004314923 @default.
- W3183360408 cites W2005248738 @default.
- W3183360408 cites W2006754278 @default.
- W3183360408 cites W2007244362 @default.
- W3183360408 cites W2007872313 @default.
- W3183360408 cites W2009478289 @default.
- W3183360408 cites W2010550564 @default.
- W3183360408 cites W2012919184 @default.
- W3183360408 cites W2015170078 @default.
- W3183360408 cites W2021810546 @default.
- W3183360408 cites W2030650261 @default.
- W3183360408 cites W2032691826 @default.
- W3183360408 cites W2033828700 @default.
- W3183360408 cites W2033885016 @default.
- W3183360408 cites W2034301098 @default.
- W3183360408 cites W2036464895 @default.
- W3183360408 cites W2036934174 @default.
- W3183360408 cites W2038468721 @default.
- W3183360408 cites W2039848901 @default.
- W3183360408 cites W2041036994 @default.
- W3183360408 cites W2042000503 @default.
- W3183360408 cites W2044993635 @default.
- W3183360408 cites W2045106215 @default.
- W3183360408 cites W2046353863 @default.
- W3183360408 cites W2064871936 @default.
- W3183360408 cites W2065575443 @default.
- W3183360408 cites W2065894898 @default.
- W3183360408 cites W2067841051 @default.
- W3183360408 cites W2069519394 @default.
- W3183360408 cites W2072451938 @default.
- W3183360408 cites W2073429636 @default.
- W3183360408 cites W2074871320 @default.
- W3183360408 cites W2075178687 @default.
- W3183360408 cites W2077001214 @default.
- W3183360408 cites W2081082836 @default.
- W3183360408 cites W2081184407 @default.
- W3183360408 cites W2083159612 @default.
- W3183360408 cites W2087328047 @default.
- W3183360408 cites W2090067193 @default.
- W3183360408 cites W2090761865 @default.
- W3183360408 cites W2096199252 @default.
- W3183360408 cites W2096579721 @default.
- W3183360408 cites W2101612342 @default.
- W3183360408 cites W2102085604 @default.
- W3183360408 cites W2103628478 @default.
- W3183360408 cites W2103649881 @default.
- W3183360408 cites W2104908670 @default.
- W3183360408 cites W2111698016 @default.
- W3183360408 cites W2115021528 @default.
- W3183360408 cites W2115852450 @default.
- W3183360408 cites W2116435487 @default.
- W3183360408 cites W2120439472 @default.
- W3183360408 cites W2128807350 @default.
- W3183360408 cites W2133388626 @default.
- W3183360408 cites W2141157756 @default.
- W3183360408 cites W2145578278 @default.
- W3183360408 cites W2147030667 @default.
- W3183360408 cites W2154867085 @default.
- W3183360408 cites W2155237820 @default.
- W3183360408 cites W2155353396 @default.
- W3183360408 cites W2157099092 @default.
- W3183360408 cites W2159036727 @default.