Influence of cardiometabolic comorbidities on myocardial function, infarction, and cardioprotection: Role of cardiac redox signaling

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3076324 14 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Influence of cardiometabolic comorbidities on myocardial function, infarction, and cardioprotection: Role of cardiac redox signaling
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
The morbidity and mortality from cardiovascular diseases (CVD) remain high. Metabolic diseases such as obesity, hyperlipidemia, diabetes mellitus (DM), non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) as well as hypertension are the most common comorbidities in patients with CVD. These comorbidities result in increased myocardial oxidative stress, mainly from increased activity of nicotinamide adenine dinucleotide phosphate oxidases, uncoupled endothelial nitric oxide synthase, mitochondria as well as downregulation of antioxidant defense systems. Oxidative and nitrosative stress play an important role in ischemia/reperfusion injury and may account for increased susceptibility of the myocardium to infarction and myocardial dysfunction in the presence of the comorbidities. Thus, while early reperfusion represents the most favorable therapeutic strategy to prevent ischemia/reperfusion injury, redox therapeutic strategies may provide additive benefits, especially in patients with heart failure. While oxidative and nitrosative stress are harmful, controlled release of reactive oxygen species is however important for cardioprotective signaling. In this review we summarize the current data on the effect of hypertension and major cardiometabolic comorbidities such as obesity, hyperlipidemia, DM, NAFLD/NASH on cardiac redox homeostasis as well as on ischemia/reperfusion injury and cardioprotection. We also review and discuss the therapeutic interventions that may restore the redox imbalance in the diseased myocardium in the presence of these comorbidities. © 2021 Elsevier Inc.
Έτος δημοσίευσης:
2021
Συγγραφείς:
Andreadou, I.
Daiber, A.
Baxter, G.F.
Brizzi, M.F.
Di Lisa, F.
Kaludercic, N.
Lazou, A.
Varga, Z.V.
Zuurbier, C.J.
Schulz, R.
Ferdinandy, P.
Περιοδικό:
FREE RADICAL BIOLOGY AND MEDICINE
Εκδότης:
W B SAUNDERS CO-ELSEVIER INC
Τόμος:
166
Σελίδες:
33-52
Λέξεις-κλειδιά:
alpha tocopherol; antidiabetic agent; antihypertensive agent; antiobesity agent; antioxidant; dipeptidyl peptidase IV inhibitor; endothelial nitric oxide synthase; flavonoid; glucagon like peptide 1; hydroxymethylglutaryl coenzyme A reductase inhibitor; nutraceutical; omega 3 fatty acid; peroxisome proliferator activated receptor gamma agonist; reduced nicotinamide adenine dinucleotide phosphate oxidase; resveratrol; sodium glucose cotransporter 2 inhibitor; synbiotic agent, antiinflammatory activity; antioxidant activity; Article; caloric restriction; cardiovascular disease; comorbidity; diabetes mellitus; down regulation; enzyme activity; exercise; heart failure; heart function; heart infarction; heart protection; heart ventricle hypertrophy; human; hyperlipidemia; hypertension; lifestyle modification; metabolic disorder; mitochondrion; myocardial ischemia reperfusion injury; nitrosative stress; nonalcoholic steatohepatitis; nonhuman; obesity; oxidative stress; pathophysiology; prevalence; redox signaling; cardiac muscle; cardiovascular disease; infarction; metabolism; oxidation reduction reaction, Cardiovascular Diseases; Humans; Infarction; Myocardium; Oxidation-Reduction; Oxidative Stress
Επίσημο URL (Εκδότης):
DOI:
10.1016/j.freeradbiomed.2021.02.012
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