Oxidative Stress Management in Cardiorenal Diseases: Focus on Novel Antidiabetic Agents, Finerenone, and Melatonin

Theofilis, Panagiotis; Vordoni, Aikaterini; Kalaitzidis, Rigas

doi:10.3390/life12101663

Cited by 9 publications

(4 citation statements)

References 171 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The endothelial cells become "sticky" when they express members of a family of immunoglobulin-like adhesion molecules that includes ICAM-1, ICAM-2, VCAM-1 and PECAM-1; this also aids in the transendothelial migration of the lymphocytes [30]. Melatonin has long been known to inhibit adhesion molecule expression on endothelial cells, which diminishes the likelihood of the occlusion of a coronary artery due to the buildup of lymphocytes [31,32] (Figure 1). Experimental evidence documents that this action of melatonin is mediated by the nuclear receptor for melatonin (RORα)/signal transducer and activator of transcription 3 (miR-223-STAT-3) signaling pathway [33].…”

Section: Melatonin and Arterial Plaque Integritymentioning

confidence: 99%

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Reiter,

Sharma,

Chuffa

et al. 2024

Life

View full text Add to dashboard Cite

Cardiovascular disease is the cause of physical infirmity and thousands of deaths annually. Typically, during heart failure, cardiomyocyte mitochondria falter in terms of energy production and metabolic processing. Additionally, inflammation and the accumulation of non-contractile fibrous tissue contribute to cardiac malfunction. Melatonin, an endogenously produced molecule, experimentally reduces the initiation and progression of atherosclerotic lesions, which are often the basis of coronary artery disease. The current review critically analyzes published data related to the experimental use of melatonin to forestall coronary artery pathologies. Collectively, these studies document melatonin’s anti-atherosclerotic actions in reducing LDL oxidation and triglyceride levels, lowering endothelial malfunction, limiting adhesion molecule formation, preventing macrophage polarization to the M1 pro-inflammatory phenotype, changing cellular metabolism, scavenging destructive reactive oxygen species, preventing the proliferation and invasion of arterial smooth muscle cells into the lesioned area, restricting the ingrowth of blood vessels from the vasa vasorum, and solidifying the plaque cap to reduce the chance of its rupture. Diabetic hyperglycemia, which aggravates atherosclerotic plaque formation, is also inhibited by melatonin supplementation in experimental animals. The potential value of non-toxic melatonin as a possible inhibitor of cardiac pathology in humans should be seriously considered by performing clinical trials using this multifunctional molecule.

show abstract

Section: Melatonin and Arterial Plaque Integritymentioning

confidence: 99%

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Reiter,

Sharma,

Chuffa

et al. 2024

Life

View full text Add to dashboard Cite

show abstract

“…SGLT2-Is may be able to improve oxidative stress and inflammation [ 119 , 120 ]. Antioxidant and anti-inflammatory effects of SGLT2 inhibition have been demonstrated in recent experimental studies at the level of the heart [ 96 , 97 ], implicating key inflammatory mediators such as the NLRP3 inflammasome and NF-κB.…”

Section: A Novel Era In Heart Failure Pharmacotherapy: Sglt2 Inhibitorsmentioning

confidence: 99%

Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors

Theofilis

Oikonomou

Tsioufis

et al. 2023

Life

Self Cite

View full text Add to dashboard Cite

Diabetes mellitus (DM) and heart failure (HF) are frequently encountered afflictions that are linked by a common pathophysiologic background. According to landmark studies, those conditions frequently coexist, and this interaction represents a poor prognostic indicator. Based on mechanistic studies, HF can be propagated by multiple pathophysiologic pathways, such as inflammation, oxidative stress, endothelial dysfunction, fibrosis, cardiac autonomic neuropathy, and alterations in substrate utilization. In this regard, DM may augment myocardial inflammation, fibrosis, autonomic dysfunction, and lipotoxicity. As the interaction between DM and HF appears critical, the new cornerstone in DM and HF treatment, sodium-glucose cotransporter-2 inhibitors (SGLT2i), may be able to revert the pathophysiology of those conditions and lead to beneficial HF outcomes. In this review, we aim to highlight the deleterious pathophysiologic interaction between DM and HF, as well as demonstrate the beneficial role of SGLT2i in this field.

show abstract

“…Type 5 is caused by other systemic diseases such as sepsis and diabetes [15]. Although a variety of factors can cause senescence-related cardiorenal interactions, a strong body of evidence indicates that oxidative stress plays a central role [14,16] via ageinduced metabolic, hemodynamic, neurohormonal, and inflammatory mechanisms, and atherosclerotic degeneration [17][18][19]. Aging is highly correlated to the process of mitochondrial dysfunction and causes the accumulation of oxidative stress in cardiomyocytes and nephrocytes [17,20,21].…”

Section: Introductionmentioning

confidence: 99%

XBP1 Modulates the Aging Cardiorenal System by Regulating Oxidative Stress

Zhang,

Zhao,

Gong

2023

Antioxidants

View full text Add to dashboard Cite

X-box binding protein 1 (XBP1) is a unique basic-region leucine zipper (bZIP) transcription factor. Over recent years, the powerful biological functions of XBP1 in oxidative stress have been gradually revealed. When the redox balance remains undisturbed, oxidative stress plays a role in physiological adaptations and signal transduction. However, during the aging process, increased cellular senescence and reduced levels of endogenous antioxidants cause an oxidative imbalance in the cardiorenal system. Recent studies from our laboratory and others have indicated that these age-related cardiorenal diseases caused by oxidative stress are guided and controlled by a versatile network composed of diversified XBP1 pathways. In this review, we describe the mechanisms that link XBP1 and oxidative stress in a range of cardiorenal disorders, including mitochondrial instability, inflammation, and alterations in neurohumoral drive. Furthermore, we propose that differing degrees of XBP1 activation may cause beneficial or harmful effects in the cardiorenal system. Gaining a comprehensive understanding of how XBP1 exerts influence on the aging cardiorenal system by regulating oxidative stress will enhance our ability to provide new directions and strategies for cardiovascular and renal safety outcomes.

show abstract

Oxidative Stress Management in Cardiorenal Diseases: Focus on Novel Antidiabetic Agents, Finerenone, and Melatonin

Cited by 9 publications

References 171 publications

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors

XBP1 Modulates the Aging Cardiorenal System by Regulating Oxidative Stress

Contact Info

Product

Resources

About