Flavine adenine dinucleotide inhibits pathological cardiac hypertrophy and fibrosis through activating short chain acyl-CoA dehydrogenase

Oxidative stress in cardiac hypertrophy: From molecular mechanisms to novel therapeutic targets

“…In other studies, the rate-limiting enzyme of fatty acid β-oxidation, short-chain acyl-CoA dehydrogenase (SCAD) is reported to negatively regulate cardiac hypertrophy and fibrosis [40]. Consistently, by increasing expression and enzyme activity of SCAD, flavin adenine dinucleotide treatment was shown to inhibit cardiomyocyte hypertrophy and cardiac fibroblast proliferation [41] that was attributed to increased fatty acid oxidation and decreased ROS production. Similarly, allylmethylsulfide, a novel sulphur metabolite of garlic was shown to attenuate cardiac hypertrophy and fibrosis by reducing oxidative stress (via reducing lipid peroxidation and improving exogenous antioxidant activity) and apoptosis in addition to stabilising extra cellular matrix components [42], likely mediated through Na + /K + -ATPase [43].…”

Gut Microbiota and Metabolites in Atrial Fibrillation Patients and Their Changes after Catheter Ablation

“…In our study, downregulation of flavin mononucleotide (FMN) and FAD in AF may be related to disordered riboflavin metabolism, which can lead to mitochondrial dysfunction by reducing energy metabolism levels ( 24 ) and may affect the normal function of the heart and increase susceptibility to AF. In addition, FAD can significantly increase the expression of short-chain acyl coenzyme A dehydrogenase and inhibit pathomyocardial hypertrophy and fibrosis ( 25 ). Inosine can induce the improvement of endothelium-dependent vasodilation, exhibit antiplatelet properties, activate endothelial nitric oxide synthase (eNOS), and reduce p38MAPK/NF-κB pathway expression in aortic tissue ( 26 ).…”

Bioinformatics Analysis of next generation sequencing data for Risk Prediction in Patients with Type 1 diabetes mellitus

“…A previous study reported that LXN (latexin) [84], LMNA (lamin A/C) [85], PFKFB3 [86], NEU1 [87], TBK1 [88], GRN (granulin precursor) [89], CTSD (cathepsin D) [90], ACADS (acyl-CoA dehydrogenase short chain) [91], IRF7 [92], S1PR1 [93], ZAP70 [94], IDH1 [95], IL15 [96], PIK3R1 [97], OSM (oncostatin M) [98], SOCS3 [99], USP21 [100], CEP19 [101], KDM2A [102], TP53 [103], BRD2 [104], ATP6 [105], BRD4 [106], COX2 [107], RPS6 [108], ND2 [109], CYTB (cytochrome b) [110] and COX1 [111] are altered expressed in obesity. Altered expression of BCL3 [112], TRAF2 [113], NEU1 [114], SNAP29 [115], AGPAT2 [116], LPCAT3 [117], ADORA2B [118], CTSD (cathepsin D) [119], ACADS (acyl-CoA dehydrogenase short chain) [120], ACAD9 [121], E4F1 [122], IRF7 [123], TAF1 [124], S1PR1 [125], RASSF1 [126], ELAC2 [127], RNF146 [128], COX15 [129], SMYD2 [130], IDH1 [131], MTO1 [132], IL15 [133], PIK3R1 [134], ASB1 [135], OSM (oncostatin M) [136], ZNF791 [137], GBA (glucosylceramidase beta) [138], SOCS3 [139], SLC39A7 [140], AKIP1 [141], AMIGO2 [142], GLUL (glutamate-ammonia ligase) [143], SEMA4D [144], KDM2A [145], TP53 [146], JARID2 [147], CTBP1 [148], ATP6 [149], RPL7 [150], HSP90AA1 [151], BRD4 [152], PSMB4 [153], COX2 [154], JUND (JunD proto-oncogene, AP-1 transcription factor subunit) [155], RPS5 [156], RACK1 […”