Matches in SemOpenAlex for { <https://semopenalex.org/work/W3149666027> ?p ?o ?g. }
- W3149666027 endingPage "101338" @default.
- W3149666027 startingPage "101338" @default.
- W3149666027 abstract "Association of diabetes with an elevated risk of cardiac failure has been clinically evident. Diabetes potentiates diastolic and systolic cardiac failure following the myocardial infarction that produces the cardiac muscle-specific microvascular complication, clinically termed as diabetic cardiomyopathy. Elevated susceptibility of diabetic cardiomyopathy is primarily caused by the generation of free radicals in the hyperglycemic milieu, compromising the myocardial contractility and normal cardiac functions with increasing redox insult, impaired mitochondria, damaged organelles, apoptosis, and cardiomyocytes fibrosis. Autophagy is essentially involved in the recycling/clearing the damaged organelles, cytoplasmic contents, and aggregates, which are frequently produced in cardiomyocytes. Although autophagy plays a vital role in maintaining the cellular homeostasis in diligent cardiac tissues, this process is frequently impaired in the diabetic heart. Given its clinical significance, accumulating evidence largely showed the functional aspects of autophagy in diabetic cardiomyopathy, elucidating its intricate protective and pathogenic outcomes. However, etiology and molecular readouts of these contrary autophagy activities in diabetic cardiomyopathy are not yet comprehensively assessed and translated. In this review, we attempted to assess the role of autophagy and its adaptations in the diabetic heart. To delineate the molecular consequences of these events, we provided detailed insights into the autophagy regulation pieces of machinery including the mTOR/AMPK, TFEB/ZNSCAN3, FOXOs, SIRTs, PINK1/Parkin, Nrf2, miRNAs, and others in the diabetic cardiomyopathy. Given the clinical significance of autophagy in the diabetic heart, we further discussed the potential pharmacotherapeutic strategies towards targeting autophagy. Taken together, the present report meticulously assessed autophagy, its adaptations, and molecular regulations in diabetic cardiomyopathy and reviewed the current autophagy-targeting strategies." @default.
- W3149666027 created "2021-04-13" @default.
- W3149666027 creator A5009823282 @default.
- W3149666027 creator A5039872482 @default.
- W3149666027 creator A5059971371 @default.
- W3149666027 creator A5065287156 @default.
- W3149666027 creator A5081233132 @default.
- W3149666027 creator A5084673116 @default.
- W3149666027 date "2021-07-01" @default.
- W3149666027 modified "2023-10-05" @default.
- W3149666027 title "Autophagy in the diabetic heart: A potential pharmacotherapeutic target in diabetic cardiomyopathy" @default.
- W3149666027 cites W1539994192 @default.
- W3149666027 cites W1715909735 @default.
- W3149666027 cites W1970149271 @default.
- W3149666027 cites W1972856187 @default.
- W3149666027 cites W1975200363 @default.
- W3149666027 cites W1976304915 @default.
- W3149666027 cites W1977916397 @default.
- W3149666027 cites W1980192302 @default.
- W3149666027 cites W1982380248 @default.
- W3149666027 cites W1982589104 @default.
- W3149666027 cites W1985026615 @default.
- W3149666027 cites W1985124617 @default.
- W3149666027 cites W1987034100 @default.
- W3149666027 cites W1987240861 @default.
- W3149666027 cites W1991511572 @default.
- W3149666027 cites W1995455049 @default.
- W3149666027 cites W1997895470 @default.
- W3149666027 cites W2007289547 @default.
- W3149666027 cites W2018559323 @default.
- W3149666027 cites W2023536633 @default.
- W3149666027 cites W2023598683 @default.
- W3149666027 cites W2027042725 @default.
- W3149666027 cites W2036152956 @default.
- W3149666027 cites W2037299745 @default.
- W3149666027 cites W2037840446 @default.
- W3149666027 cites W2041719399 @default.
- W3149666027 cites W2046664372 @default.
- W3149666027 cites W2048057768 @default.
- W3149666027 cites W2054203136 @default.
- W3149666027 cites W2065908325 @default.
- W3149666027 cites W2070658923 @default.
- W3149666027 cites W2071062711 @default.
- W3149666027 cites W2072361357 @default.
- W3149666027 cites W2073182272 @default.
- W3149666027 cites W2075504962 @default.
- W3149666027 cites W2081706292 @default.
- W3149666027 cites W2082402714 @default.
- W3149666027 cites W2082906971 @default.
- W3149666027 cites W2086892760 @default.
- W3149666027 cites W2088538972 @default.
- W3149666027 cites W2089122115 @default.
- W3149666027 cites W2091210052 @default.
- W3149666027 cites W2096317893 @default.
- W3149666027 cites W2097693006 @default.
- W3149666027 cites W2099283141 @default.
- W3149666027 cites W2101080348 @default.
- W3149666027 cites W2102614059 @default.
- W3149666027 cites W2112254297 @default.
- W3149666027 cites W2117119983 @default.
- W3149666027 cites W2118144377 @default.
- W3149666027 cites W2119551073 @default.
- W3149666027 cites W2128536736 @default.
- W3149666027 cites W2129155846 @default.
- W3149666027 cites W2131444090 @default.
- W3149666027 cites W2131520853 @default.
- W3149666027 cites W2131646286 @default.
- W3149666027 cites W2134907909 @default.
- W3149666027 cites W2142461094 @default.
- W3149666027 cites W2149788817 @default.
- W3149666027 cites W2151864871 @default.
- W3149666027 cites W2171155178 @default.
- W3149666027 cites W2200202512 @default.
- W3149666027 cites W2294575394 @default.
- W3149666027 cites W2294945370 @default.
- W3149666027 cites W2319656552 @default.
- W3149666027 cites W2339207243 @default.
- W3149666027 cites W2396931055 @default.
- W3149666027 cites W2425644022 @default.
- W3149666027 cites W2463432899 @default.
- W3149666027 cites W2467322882 @default.
- W3149666027 cites W2515285615 @default.
- W3149666027 cites W2532576306 @default.
- W3149666027 cites W2545883892 @default.
- W3149666027 cites W2554702493 @default.
- W3149666027 cites W2556584415 @default.
- W3149666027 cites W2562899840 @default.
- W3149666027 cites W2572840791 @default.
- W3149666027 cites W2595321482 @default.
- W3149666027 cites W2601616556 @default.
- W3149666027 cites W2601655543 @default.
- W3149666027 cites W2605404328 @default.
- W3149666027 cites W2611971693 @default.
- W3149666027 cites W2612482748 @default.
- W3149666027 cites W2614434863 @default.
- W3149666027 cites W2747174776 @default.
- W3149666027 cites W2750394635 @default.
- W3149666027 cites W2752112633 @default.