Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000537144> ?p ?o ?g. }
- W2000537144 endingPage "62" @default.
- W2000537144 startingPage "47" @default.
- W2000537144 abstract "The heart is a dynamic organ capable of significant architectural remodeling, cellular adaptations, and molecular reprogramming following both physiologic and pathologic stimulation. These whole organ and cellular adaptations are typically initiated by stress-responsive signaling pathways, which serve as central transducers of cardiac hypertrophic growth and/or ventricular dilation. In addition to initiating and maintaining phenotypic alterations in cardiac structure and function, stress-responsive signaling pathways have also been implicated in affecting the decision of myocytes to either survive or undergo programmed cell death (apoptosis). Indeed, necrosis or apoptosis of individual myocytes has become appreciated as yet another maladaptive event that negatively impacts the myocardium and its propensity towards failure. Here we will discuss the known associations between select stress-induced and neuroendocrine-mediated signaling pathways and regulation of cardiac myocyte survival or cell death. These signaling pathways include the extracellular signal-regulated protein kinases (ERK), p38 mitogen-activated protein kinases (MAPK), c-Jun NH2-terminal kinases (JNK), protein kinase C (PKC) isoforms, the protein phosphatase calcineurin, as well as a select group of additional kinases such as Janus kinase (JAK). While a fair amount of discordance exists in the literature, we will weigh evidence that largely suggests a pro-apoptotic regulatory role for the p38 mitogen-activated protein kinase, JNK, and PKCdelta, yet an anti-apoptotic regulatory role for ERK, PKCepsilon, JAK, and calcineurin in the myocardium." @default.
- W2000537144 created "2016-06-24" @default.
- W2000537144 creator A5071684244 @default.
- W2000537144 creator A5075550603 @default.
- W2000537144 date "2005-01-01" @default.
- W2000537144 modified "2023-09-30" @default.
- W2000537144 title "STRESS signaling pathways that modulate cardiac myocyte apoptosis" @default.
- W2000537144 cites W133296140 @default.
- W2000537144 cites W1530104357 @default.
- W2000537144 cites W1530284699 @default.
- W2000537144 cites W1569503463 @default.
- W2000537144 cites W1572174728 @default.
- W2000537144 cites W1582753616 @default.
- W2000537144 cites W1591646293 @default.
- W2000537144 cites W1596495551 @default.
- W2000537144 cites W1598829273 @default.
- W2000537144 cites W1608360403 @default.
- W2000537144 cites W1788426598 @default.
- W2000537144 cites W1806836340 @default.
- W2000537144 cites W1823288226 @default.
- W2000537144 cites W1963942415 @default.
- W2000537144 cites W1964152667 @default.
- W2000537144 cites W1964476797 @default.
- W2000537144 cites W1967526945 @default.
- W2000537144 cites W1967894078 @default.
- W2000537144 cites W1967912613 @default.
- W2000537144 cites W1970579406 @default.
- W2000537144 cites W1970856815 @default.
- W2000537144 cites W1971072760 @default.
- W2000537144 cites W1972101997 @default.
- W2000537144 cites W1972680803 @default.
- W2000537144 cites W1973098476 @default.
- W2000537144 cites W1973466803 @default.
- W2000537144 cites W1976385326 @default.
- W2000537144 cites W1978559408 @default.
- W2000537144 cites W1978813721 @default.
- W2000537144 cites W1978983255 @default.
- W2000537144 cites W1979097982 @default.
- W2000537144 cites W1982421412 @default.
- W2000537144 cites W1982499214 @default.
- W2000537144 cites W1982936505 @default.
- W2000537144 cites W1985412375 @default.
- W2000537144 cites W1986098328 @default.
- W2000537144 cites W1986191342 @default.
- W2000537144 cites W1989823141 @default.
- W2000537144 cites W1991163286 @default.
- W2000537144 cites W1991274073 @default.
- W2000537144 cites W1991447679 @default.
- W2000537144 cites W1991545343 @default.
- W2000537144 cites W1992738986 @default.
- W2000537144 cites W1994673402 @default.
- W2000537144 cites W2001333805 @default.
- W2000537144 cites W2001634583 @default.
- W2000537144 cites W2001959880 @default.
- W2000537144 cites W2002663912 @default.
- W2000537144 cites W2003805549 @default.
- W2000537144 cites W2005909927 @default.
- W2000537144 cites W2008046168 @default.
- W2000537144 cites W2008242443 @default.
- W2000537144 cites W2008622025 @default.
- W2000537144 cites W2009797078 @default.
- W2000537144 cites W2013167680 @default.
- W2000537144 cites W2015157179 @default.
- W2000537144 cites W2015157788 @default.
- W2000537144 cites W2016236878 @default.
- W2000537144 cites W2016302829 @default.
- W2000537144 cites W2016364696 @default.
- W2000537144 cites W2018221682 @default.
- W2000537144 cites W2020007683 @default.
- W2000537144 cites W2020428280 @default.
- W2000537144 cites W2020858778 @default.
- W2000537144 cites W2022265177 @default.
- W2000537144 cites W2023211139 @default.
- W2000537144 cites W2023494473 @default.
- W2000537144 cites W2025620168 @default.
- W2000537144 cites W2028151158 @default.
- W2000537144 cites W2029774465 @default.
- W2000537144 cites W2031108838 @default.
- W2000537144 cites W2032580133 @default.
- W2000537144 cites W2032864246 @default.
- W2000537144 cites W2034720665 @default.
- W2000537144 cites W2037945038 @default.
- W2000537144 cites W2038171431 @default.
- W2000537144 cites W2039407113 @default.
- W2000537144 cites W2042928324 @default.
- W2000537144 cites W2044959710 @default.
- W2000537144 cites W2046846631 @default.
- W2000537144 cites W2047067372 @default.
- W2000537144 cites W2048404789 @default.
- W2000537144 cites W2051890388 @default.
- W2000537144 cites W2053362512 @default.
- W2000537144 cites W2053383702 @default.
- W2000537144 cites W2056009784 @default.
- W2000537144 cites W2057479530 @default.
- W2000537144 cites W2058367692 @default.
- W2000537144 cites W2058588605 @default.
- W2000537144 cites W2060725618 @default.
- W2000537144 cites W2062128738 @default.