New insights into the role of melatonin in diabetic cardiomyopathy

Huang, Keming; Luo, Xianling; Zhong, Yi; Deng, Li; Feng, Jian

doi:10.1002/prp2.904

Cited by 16 publications

(3 citation statements)

References 274 publications

(474 reference statements)

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“…Moreover, a major aspect of the melatonin's ability to shelter cardiomyocytes from elevated glucose levels during diabetes likely involves preservation of mitochondrial function [93,94]. The collective findings indicate that melatonin's protection of the heart from deterioration under diabetic cardiomyopathic conditions is unequivocal and multifunctional [95][96][97]. Considering the serious nature of cardiovascular and cardiac damage in individuals suffering with T2D, melatonin supplementation could be considered a reasonable and likely effective means of combating this seriously destructive condition (Figure 5).…”

Section: Melatonin and Diabetic Cardiomyopathymentioning

confidence: 99%

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Reiter,

Sharma,

Chuffa

et al. 2024

Life

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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.

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Section: Melatonin and Diabetic Cardiomyopathymentioning

confidence: 99%

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Reiter,

Sharma,

Chuffa

et al. 2024

Life

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“…Multiple investigations have also shown that SIRT1 activation is neuroprotective in DN in part by enhancing mitochondrial bioenergetics and autophagy [21,22]. Additional studies have also demonstrated that AMPK and SIRT1 help to reduce DN by improving mitochondrial function through the PGC-1α and Nrf2 axis [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Cannabidiol and Beta-Caryophyllene Combination Attenuates Diabetic Neuropathy by Inhibiting NLRP3 Inflammasome/NFκB through the AMPK/SIRT3/Nrf2 Axis

Khan,

Kaur,

Rishi

et al. 2024

Preprint

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Background In this study we investigated in detail the role of cannabidiol (CBD), Beta-caryophyllene (BC), or their combinations in diabetic peripheral neuropathy (DN). The key factors that contribute to DN include mitochondrial dysfunction, inflammation, and oxidative stress. Methods Briefly, Streptozotocin (STZ) (55 mg/kg) was injected intraperitoneally to induce DN in Sprague Dawley rats and performed procedures including Randall Sellito Calipers, Von Frey Aesthesiometer, hot plate, and cold plate methods to determine mechanical and thermal hyperalgesia in vivo. The blood flow to the nerves was assessed by using the Laser Doppler device. Schwann cells were exposed to high glucose (HG) at a dose of 30 mM to induce hyperglycemia and DCFDA, JC1 & Mitosox staining were done to determine mitochondrial membrane potential, reactive oxygen species and mitochondrial superoxides in-vitro. The rats were administered i.p with BC (30mg/kg), CBD (15mg/kg), or combination while Schwann cells were treated with 3.65 µM CBD, 75 µM BC, or combination to assess their role in DN amelioration. Results Our results revealed that exposure to BC and CBD diminished HG-induced hyperglycemia in Schwann cells, in part, through reducing mitochondrial membrane potential, reactive oxygen species and mitochondrial superoxides. Further, BC and CBD combination treatment in-vivo could prevent the deterioration of mitochondrial quality control system by promoting autophagy and mitochondrial biogenesis while improving blood flow. CBD and BC treatments also reduced pain hypersensitivity to hyperalgesia and allodynia with increased antioxidant and anti-inflammatory action in diabetic rats. These in vivo effects were attributed to significant upregulation of AMPK, SIRT3, Nrf2, PINK1, PARKIN, LC3B, Beclin1 and TFAM functions while downregulation of NLRP3 inflammasome, NFκB, COX2 and p62 activity was noted as determined by western blotting. Conclusion the present studies demonstrated that STZ & HG induced oxidative and nitrosative stress play a crucial role in the pathogenesis of diabetic neuropathy. We find, for the first time, that CBD and BC combination ameliorate DN via modulating the mitochondrial quality control system.

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“…Some patients have a hyperglycemia-induced myocardial injury but do not have high blood pressure or coronary artery disease. This disease, termed diabetic cardiomyopathy ( 3 ), is currently of considerable interest among researchers ( 4 ). The underlying mechanisms of hyperglycemia-induced myocardial injury include cardiac inflammation, increased reactive oxygen species (ROS), interstitial fibrosis, and cardiac cell apoptosis ( 2 , 5 ).…”

Section: Introductionmentioning

confidence: 99%

Naringenin ameliorates myocardial injury in STZ-induced diabetic mice by reducing oxidative stress, inflammation and apoptosis via regulating the Nrf2 and NF-κB signaling pathways

Wang

Sun

et al. 2022

Front. Cardiovasc. Med.

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Diabetes-induced myocardial damage leads to diabetic cardiomyopathy and is closely associated with the generation of oxidative stress and inflammation. Naringenin (NG) exhibits antioxidant and anti-inflammatory effects. However, whether NG has cardioprotective effects against diabetic cardiomyopathy by regulating oxidative stress and inflammation remains unknown. This study investigated the effect of NG on diabetic cardiomyopathy based on an analysis of streptozotocin (STZ)-induced type 1 diabetic mice. The results indicated that NG reduced cardiac fibrosis and cardiomyocyte apoptosis in this diabetic model, accompanied by reduced blood glucose. NG inhibited pro-inflammatory cytokines, the level of reactive oxygen species and the expression of nuclear factor kappa-B (NF-κB), whereas the expression of antioxidant enzymes and nuclear factor erythroid 2-related factor 2 (Nrf2) were greatly enhanced by NG. Furthermore, in high glucose-treated H9C2 myocardial cells, NG effectively reduced cell apoptosis by inhibiting the formation of reactive oxygen species and pro-inflammatory cytokines. NG's antioxidant and anti-inflammatory activities were mechanistically associated with NF-κB inhibition and Nrf2 activation in animal and cell experiments. Data analysis showed that NG could regulate Nrf2 and NF-κB pathways to protect against diabetes-induced myocardial damage by reducing oxidative stress and inhibiting inflammation.

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New insights into the role of melatonin in diabetic cardiomyopathy

Cited by 16 publications

References 274 publications

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

Cannabidiol and Beta-Caryophyllene Combination Attenuates Diabetic Neuropathy by Inhibiting NLRP3 Inflammasome/NFκB through the AMPK/SIRT3/Nrf2 Axis

Naringenin ameliorates myocardial injury in STZ-induced diabetic mice by reducing oxidative stress, inflammation and apoptosis via regulating the Nrf2 and NF-κB signaling pathways

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