Table 1.

Overview of ROS, oxidative stress and cardiac structure and function in DbCM.

Diabetes Model	ROS/Oxidative Stress	Cardiac Function/Structure	Author
Permeabilized atrial myofibers from T2D patients (LVEF >30%)	↑ mitochondrial H2O2 emission ↓ GSH/GSSG ratio ↑HNE, 3-NT	↔ systolic function	Anderson [74]
Obese T2D patients without HF, CAD and hypertension	↑ glycogen ↑ HO-1, NQO1	↑ LV hypertrophy ↑ myocardial fibrosis	Li [234]
Right atrial myocardium from diabetic patients without signs of CM	↑ ROS levels ↑ MnSOD, CAT; ↔ Cu-ZnSOD activities	↓ mitochondrial function ↑ contractile dysfunction of atrial without signs ↓ complex I activity in obese/diabetic individuals	Montaigne [77]
Human diabetic hearts	↓ NRF2 staining		Tan [233]
STZ-induced T1D guinea pigs	↑ ROS levels; ↔ GSH ↓ basal complex II state 4H2O2 emission ↔ SOD, GSH-Px, PRX, GSH, TRXR1/2, CAT, TRX1/2 ↑ oxidant-challenged H2O2 emission	↓ complex II and IV state 3 VO2 ↓ ADP phosphorylation rates	Tocchetti [38]
STZ-induced T1D rats	↑ O2•− ; ↓ complex I H2O2 production; ↑/↓ H2O2 production; ↑ CM ROS, TBARS, MDA, lipid peroxide, protein carbonyl, 8-iso PGF2α, HNE-adduct of SDH subunit, NT of SCOT; ↓ mitochondrial MDA ↓ GSH; ↑ GSH conjugate efflux; ↔ γ-GSC mRNA, GSR activity; ↑ GSH/GSSG ratio ↑ p22phox, NOX4 mRNA ↑/↓ SOD content; ↑ CAT; ↔ CuZn-SOD, GSH-Px activities; MnSOD, GSH-Px, PRX3 protein	↑/↓ cardiac hypertrophy ↓ systolic and diastolic function ↑ cardiac fibrosis, apoptosis ↑ mitochondrial dysfunction; ↓ mitochondrial transcription/translation, respiration ↑ respiratory uncoupling ↓ ETC proteins; complex I, SDH, SCOT activities	Singh [37], Ghosh [35], Kanazawa [36] Kakkar [39], da Silva [40] Hamblin [41], Wohaieb [43], Herlein [44], Lashin [42], Turko [180], Turko [262], Guo [126]
STZ-induced T1D mice	↑ ROS generation in IFM, NT, MDA, 4-HNE; AGE protein; ↔ protein carbonyl ↓ GSH/GSSG ratio ↑ NOX2 mRNA ↑ OGT, OGA mRNA; O-GlcNAc	↔ cardiac hypertrophy ↓ diastolic function; contractility ↑ fibrosis ↑ DNA fragmentation ↑ Ca2+-handling dysfunction ↓ mitochondrial respiration	Dabkowski [24], Ceylan-Isik [25], De Blasio [26]
ALX-induced T1D rats	↑ intracellular ROS, MDA, protein carbonylation, lipid peroxide levels, ↑ NT of mitochondrial proteins; ↓ TBARS [51] ↓ GSH/GSSG ratio ↑ XO activity ↓ SOD, CAT, GST, GSR, GSH-Px activities	↑ CM disorganization ↓ mitochondrial membrane potential; ↑ cytosolic cytochrome c translocation ↑ apoptosis ↓ stimulated SCOT, complex I activities	Das [45], Genet [46], Parinandi [51], Turko [47]
OVE26 T1D mice	↓ mitochondrial GSH; ↑ GSSG; ↔ GSH content ↑ CAT activity	↑ CM morphological damage ↑ mitochondrial area, number, protein, mtDNA ↓ RCR, state 3 respiration, P/O, state 4 respiration	Shen [48], Shen [31], Liang [50]
ISDBB T1D rats	↑ CAT, GSSG reductase activities ↑ GSH content		Wohaieb [49]
Akita T1D mice	↓ mitochondrial H2O2 production; ↔ ROS ↔ SOD2, PRDX3 mRNA/protein	↔ O2 consumption	Bugger [52]
db/db obese/T2D mice	↑ total ROS, O2•− , ONOO•-, 4-HNE, 8OHdG, MDA ↓ GSH, GSH/GSSG ratio ↑ gp91phox, NOX1 mRNA; ↑ PRX5; ↔ SOD2 proteins ↓ OGG-1 activity	↑ cardiac remodeling ↓ systolic function ↑ apoptosis ↑ myocardial lipotoxicity ↓ complex III activity, ATP production, ATP/ADP ratio	Mariappan [56], Das [58], Pan [59], Li [234]
ob/ob obese pre-T2D mice	↓ GSH/GSSG; ↑ MDA, protein carbonyl ↑ p47phox, gp91phox protein		Li [114]
ZDF T2D rats	↑ ROS, MDA, protein carbonylation, ↑ CAT, GSH-Px, Cu/Zn-SOD, Mn-SOD ↑ GSH, GST, GSR ↑ HO-1, iNOS protein	↑ LV hypertrophy ↓ complex I, IV activities ↓ cytochrome c oxidase subunit 1	Raza [60], Conti [400]
fa/fa T2D rats	↑ TBARS, lipid hydroperoxides, GSH; ↔ O2•− formation ↑ SOD activities		Vincent [61]
HFD-fed T2D rats	↑ TBARS, lipid hydroperoxides, GSH; ↔ O2•− formation ↑ iNOS synthase, NO ↑ SOD activities		Vincent [61], Banerjee [62]
fructose-induced pre-T2D rats	↔ MDA, 3-NT ↑ XO activity; ↑ PRX6; ↓ SOD2 mRNA	↑/↓ ETC mRNA ↑ apoptosis	Szűcs [63], Fan [129]
HFD-fed/STZ-induced pre-T2D [64] rats, mice [234] or miniswine [65]	↑ mitochondrial ROS; total and NOX-stimulated O2•− production ↓ NO production; ↑ eNOS uncoupling ↑ NRF2 pathway activation	↑ diastolic and systolic dysfunction ↑ LV mass/remodeling; CM size ↑ myocardial fibrosis, apoptosis ↑ myocardial lipotoxicity	Koncsos [64], Heinonen [65], Li [234]
Goto-Kakizaki T2D rats	↑ MDA ↓ GSH, CoQ9; ↔ α-tocopherol, CoQ10, Vitamin E	↑ O2 consumption	Santos [68]