FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2147019080> ?p ?o ?g. }

• W2147019080 endingPage "5526" @default.
• W2147019080 startingPage "5510" @default.
• W2147019080 abstract "Mitochondria are the organelles producing most of the energy and play important roles in a variety of biochemical functions in human cells. Mitochondrial defects can cause ATP deficiency and overproduction of reactive oxygen species, which are the major hallmarks of mitochondrial diseases. Abundant evidence has suggested that mitochondrial dysfunction-elicited oxidative stress can play an important role in the pathogenesis and progression of mitochondrial diseases. Mitochondria can respond to energy deficiency by the retrograde signaling to trigger a number of molecular events to help the human cells to cope with physiological or environmental changes. In this article, we first describe oxidative stress-induced cellular responses including metabolic adaptation, compensatory increase of mitochondrial biogenesis, upregulation of antioxidant enzymes, and alteration of protein acetylation in human cells with mitochondrial dysfunction. In this regard, we review recent findings to elucidate the mechanisms by which human cells motivate their mitochondria and the antioxidant defense system to respond to energy deficiency and oxidative stress, which contribute to the adaptive metabolic reprogramming in mitochondrial diseases. In addition, we emphasize the critical role of the activation of AMPK, Sirt1 and Sirt3 in the metabolic adaptation of human cells harboring mitochondrial DNA mutations. Recent studies have revealed that AMPK and sirtuins-mediated signaling pathways are involved in metabolic reprogramming, which is effected by upregulation of antioxidant defense system and mitochondrial protein acetylation, in human cells with mitochondrial dysfunction. Finally, we discuss several potential modulators of bioenergetic function such as coenzyme Q10, mitochondria-targeting antioxidants, resveratrol, and L-carnitine based on recent findings from studies on human cells and animal models of mitochondrial diseases. Elucidation of the signaling pathway of this adaptive response to oxidative stress triggered by mitochondrial dysfunction may enable us to gain a deeper insight into the communication between mitochondria and the nucleus and guide us to develop novel therapeutic agents for effective treatment of mitochondrial diseases. Keywords: AMPK, antioxidant enzyme, metabolic adaptation, mitochondrial disease, mtDNA mutation, oxidative stress, sirtuin." @default.
• W2147019080 created "2016-06-24" @default.
• W2147019080 creator A5000776771 @default.
• W2147019080 creator A5025862687 @default.
• W2147019080 creator A5042206451 @default.
• W2147019080 date "2014-09-12" @default.
• W2147019080 modified "2023-09-30" @default.
• W2147019080 title "Metabolic Reprogramming of Human Cells in Response to Oxidative Stress: Implications in the Pathophysiology and Therapy of Mitochondrial Diseases" @default.
• W2147019080 cites W1482169712 @default.
• W2147019080 cites W1500939659 @default.
• W2147019080 cites W1526834337 @default.
• W2147019080 cites W1528682921 @default.
• W2147019080 cites W153393150 @default.
• W2147019080 cites W1535022915 @default.
• W2147019080 cites W1569055531 @default.
• W2147019080 cites W1589421810 @default.
• W2147019080 cites W1603646385 @default.
• W2147019080 cites W1611338991 @default.
• W2147019080 cites W1648000881 @default.
• W2147019080 cites W179805595 @default.
• W2147019080 cites W1812782019 @default.
• W2147019080 cites W1941663272 @default.
• W2147019080 cites W1964032030 @default.
• W2147019080 cites W1964483580 @default.
• W2147019080 cites W1967901428 @default.
• W2147019080 cites W1968408636 @default.
• W2147019080 cites W1969156376 @default.
• W2147019080 cites W1970009760 @default.
• W2147019080 cites W1972393069 @default.
• W2147019080 cites W1973455163 @default.
• W2147019080 cites W1973620047 @default.
• W2147019080 cites W1973925468 @default.
• W2147019080 cites W1974582070 @default.
• W2147019080 cites W1975332428 @default.
• W2147019080 cites W1975619206 @default.
• W2147019080 cites W1979815517 @default.
• W2147019080 cites W1982764052 @default.
• W2147019080 cites W1983465246 @default.
• W2147019080 cites W1983642028 @default.
• W2147019080 cites W1983726222 @default.
• W2147019080 cites W1984695384 @default.
• W2147019080 cites W1985730861 @default.
• W2147019080 cites W1987224043 @default.
• W2147019080 cites W1988664434 @default.
• W2147019080 cites W1988834592 @default.
• W2147019080 cites W1991730412 @default.
• W2147019080 cites W1992153206 @default.
• W2147019080 cites W1993397999 @default.
• W2147019080 cites W1994153334 @default.
• W2147019080 cites W1995631432 @default.
• W2147019080 cites W1995754480 @default.
• W2147019080 cites W1996583908 @default.
• W2147019080 cites W1998776259 @default.
• W2147019080 cites W2000205368 @default.
• W2147019080 cites W2001604240 @default.
• W2147019080 cites W2002333610 @default.
• W2147019080 cites W2004415657 @default.
• W2147019080 cites W2006115379 @default.
• W2147019080 cites W2006491574 @default.
• W2147019080 cites W2007541295 @default.
• W2147019080 cites W2008663101 @default.
• W2147019080 cites W2009280475 @default.
• W2147019080 cites W2009826707 @default.
• W2147019080 cites W2013723759 @default.
• W2147019080 cites W2013841882 @default.
• W2147019080 cites W2017194280 @default.
• W2147019080 cites W2017741706 @default.
• W2147019080 cites W2018961056 @default.
• W2147019080 cites W2021784772 @default.
• W2147019080 cites W2025455509 @default.
• W2147019080 cites W2028935677 @default.
• W2147019080 cites W2029997359 @default.
• W2147019080 cites W2030227512 @default.
• W2147019080 cites W2032368297 @default.
• W2147019080 cites W2032434211 @default.
• W2147019080 cites W2033625307 @default.
• W2147019080 cites W2033898418 @default.
• W2147019080 cites W2034470301 @default.
• W2147019080 cites W2035543709 @default.
• W2147019080 cites W2039045409 @default.
• W2147019080 cites W2039374791 @default.
• W2147019080 cites W2039717666 @default.
• W2147019080 cites W2040625305 @default.
• W2147019080 cites W2043595793 @default.
• W2147019080 cites W2044434127 @default.
• W2147019080 cites W2045358555 @default.
• W2147019080 cites W2047673408 @default.
• W2147019080 cites W2049266192 @default.
• W2147019080 cites W2049547722 @default.
• W2147019080 cites W2050363846 @default.
• W2147019080 cites W2050604139 @default.
• W2147019080 cites W2050626041 @default.
• W2147019080 cites W2052751736 @default.
• W2147019080 cites W2052973017 @default.
• W2147019080 cites W2053039257 @default.
• W2147019080 cites W2053176849 @default.
• W2147019080 cites W2055775240 @default.
• W2147019080 cites W2056605533 @default.

• next