Diabetic Cardiomyopathy

Paolillo, Stefania; Marsico, Fabio; Prastaro, Maria; Renga, F.; Esposito, Luca; Martino, Fabiana De; Napoli, Pierfrancesco Di; Esposito, Immacolata; Ambrosio, Antonio; Ianniruberto, Monica; Mennella, R.; Paolillo, Roberta; Gargiulo, Paola

doi:10.1016/j.hfc.2019.02.003

Cited by 155 publications

(85 citation statements)

References 36 publications

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“…Hyperglycemia, systemic and cardiac insulin resistance, increased free fatty acid (FFA) levels, renin-angiotensin-aldosterone system (RAAS) activation, sympathetic dysfunction, myocardial inflammation, oxidative stress, remodeling and fibrosis are factors that contribute to the development of CM. However, the exact pathophysiological mechanisms remain unclear [116].…”

Section: Cardiomyopathiesmentioning

confidence: 99%

Mitophagy in Cardiovascular Diseases

Morciano

Patergnani

Bonora

et al. 2020

JCM

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Cardiovascular diseases are one of the leading causes of death. Increasing evidence has shown that pharmacological or genetic targeting of mitochondria can ameliorate each stage of these pathologies, which are strongly associated with mitochondrial dysfunction. Removal of inefficient and dysfunctional mitochondria through the process of mitophagy has been reported to be essential for meeting the energetic requirements and maintaining the biochemical homeostasis of cells. This process is useful for counteracting the negative phenotypic changes that occur during cardiovascular diseases, and understanding the molecular players involved might be crucial for the development of potential therapies. Here, we summarize the current knowledge on mitophagy (and autophagy) mechanisms in the context of heart disease with an important focus on atherosclerosis, ischemic heart disease, cardiomyopathies, heart failure, hypertension, arrhythmia, congenital heart disease and peripheral vascular disease. We aim to provide a complete background on the mechanisms of action of this mitochondrial quality control process in cardiology and in cardiac surgery by also reviewing studies on the use of known compounds able to modulate mitophagy for cardioprotective purposes.

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Section: Cardiomyopathiesmentioning

confidence: 99%

Mitophagy in Cardiovascular Diseases

Morciano

Patergnani

Bonora

et al. 2020

JCM

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“…Diabetic cardiomyopathy (DCM) is a pathological condition of the heart observed in subjects with diabetes, and it is independent of other cardiovascular pathologies such as hypertension, ischemic heart injury, coronary artery disease, and congenital heart diseases. DCM is a major cause of heart failure [4,5]. The progression of diabetes mellitus to diabetic cardiomyopathy involves the interplay of several mechanisms: oxidative damage, inflammation, apoptosis, mitochondrial dysfunction, and overactivation of Raas (Renin-angiotensin aldosterone system), as illustrated in Figure 1 [6,7].…”

Section: Introductionmentioning

confidence: 99%

Effects of Anchomanes difformis on Inflammation, Apoptosis, and Organ Toxicity in STZ-Induced Diabetic Cardiomyopathy

et al. 2020

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Persistent hyperglycemia is known to cause enhanced generation of reactive oxygen species in diabetes. Several inflammatory cytokines are induced by oxidative stress, and their release also leads to increased oxidative stress; this makes oxidative stress one of the important factors in the development of chronic inflammation and other immune responses. These have been implicated in the development of diabetic complications such as nephropathy and cardiomyopathy. Anchomanes difformis has been shown to possess antioxidant and anti-inflammatory potentials. The present study investigated the immunomodulatory potential and the antiapoptotic ability of Anchomanes difformis to ameliorate heart toxicity and injury in type II diabetes. Two weeks of fructose (10%) administration followed by single intraperitoneal injection of streptozotocin (40 mg/kg) were used to induce type II diabetes in male Wistar rats. Leaf extract (aqueous) of Anchomanes difformis (200 and 400 mg/kg) was administered orally for six weeks. Blood glucose concentrations and body weights before and after interventions were determined. Interleukin (IL)-1β, IL-6, IL-10, IL-18, monocyte chemoattractant protein 1 (MCP-1), and tumor necrosis factor alpha (TNFα) were measured in the heart homogenates. Catalase (CAT), superoxide dismutase (SOD), total protein, oxygen radical absorbance capacity (ORAC), ferric reducing antioxidant power (FRAP), thiobarbituric acid reactive substances (TBARS), and heart-type fatty acid-binding protein (H-FABP) levels were determined. Expressions of transcription factors (Nrf 2 and NFkB/p65) and apoptotic markers were also investigated in the heart. Anchomanes difformis administration reduced pro-inflammatory cytokines, increased anti-inflammatory markers, and enhanced antioxidant defense in the heart of diabetic treated animals. Anchomanes difformis is a new, promising therapeutic agent that can be explored for the treatment of pathological conditions associated with immune responses and will be a useful tool in the management of associated diabetic complications.

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“…[ 19 ] Previous studies found that HG‐induced myocardial cell injury and apoptosis play a key role in the development of diabetic cardiomyopathy. [ 20,21 ]…”

Section: Discussionmentioning

confidence: 99%

Spiraeoside protects human cardiomyocytes against high glucose‐induced injury, oxidative stress, and apoptosis by activation of PI3K/Akt/Nrf2 pathway

Zhang

et al. 2020

J Biochem & Molecular Tox

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The present study aimed to explore the effect of spiraeoside, an active quercetin glucoside, on diabetic cardiomyopathy in vitro. Our results showed that spiraeoside attenuated high glucose (HG)-induced reduction of cell viability and increased myocardial enzymes lactate dehydrogenase and aspartate aminotransferase in AC16 cells. Spiraeoside exerted antioxidant activity in HG-induced AC16 cells as spiraeoside inhibited reactive oxygen species and malondialdehyde production and increased activities of superoxide dismutase, glutathione peroxidase, and catalase. Spiraeoside prevented HG-induced apoptosis of AC16 cells. HG stimulation-caused the decrease in the expression levels of p-Akt, nuclear Nrf2, and HO-1 was elevated after spiraeoside treatment in AC16 cells. However, the effects of spiraeoside were reversed by LY294002. In conclusion, spiraeoside protected AC16 cells against HG-induced oxidative stress, cell injury, and apoptosis. The protective effect of spiraeoside was regulated by the PI3K/Akt/Nrf2 signaling pathway.

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Diabetic Cardiomyopathy

Cited by 155 publications

References 36 publications

Mitophagy in Cardiovascular Diseases

Mitophagy in Cardiovascular Diseases

Effects of Anchomanes difformis on Inflammation, Apoptosis, and Organ Toxicity in STZ-Induced Diabetic Cardiomyopathy

Spiraeoside protects human cardiomyocytes against high glucose‐induced injury, oxidative stress, and apoptosis by activation of PI3K/Akt/Nrf2 pathway

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