Abnormalities of glucose and lipid metabolism in myocardial ischemia-reperfusion injury

Tian, Hao; Zhao, Xiaoshuai; Zhang, Yuxi; Xia, Zhongyuan

doi:10.1016/j.biopha.2023.114827

Cited by 23 publications

(8 citation statements)

References 140 publications

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“…Previous studies further reported that exposure to BFRs in serum was related to significant enrichment of genes and metabolomic markers involved in cellular respiration and lipid metabolism ( 41 , 42 ). Glucose metabolism and lipid metabolism are vital in regulating myocardial energy metabolism ( 43 ). Therefore, metabolism reprogramming might be a potential mechanism by which BFRs contribute to CVD.…”

Section: Discussionmentioning

confidence: 99%

Single and combined association between brominated flame retardants and cardiovascular disease: a large-scale cross-sectional study

Yin,

Xu,

Zou

et al. 2024

Front. Public Health

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IntroductionThe single and combined association between brominated flame retardants (BFRs) and cardiovascular diseases (CVD) has remained unelucidated. This research aimed at exploring the associations between mixture of BFRs and CVD.MethodsThis research encompassed adult participants from the National Health and Nutrition Examination Survey in 2005–2016. The weighted quantile sum (WQS) model and quantile g-computation (QGC) model were applied to examine the combined effects of BFRs mixture on CVD.ResultsIn this research, overall 7,032 individuals were included. In comparison with the lowest quartile, the highest quartile of PBB153 showed a positive association with CVD, with odds ratio (OR) values and 95% confidence intervals (CI) of 19.2 (10.9, 34.0). Furthermore, the acquired data indicated that PBB153 (OR: 1.23; 95% CI: 1.02, 1.49), PBB99 (OR: 1.29; 95% CI: 1.06, 1.58), and PBB154 (OR: 1.29; 95% CI: 1.02, 1.63) were linked to congestive heart failure. PBB153 was also related to coronary heart disease (OR: 1.29; 95% CI: 1.06, 1.56). Additionally, a positive correlation between the BFRs mixture and CVD (positive model: OR: 1.23; 95% CI: 1.03, 1.47) was observed in the weighted quantile sum (WQS) model and the quantile g-computation (QGC) model.DiscussionTherefore, exposure to BFRs has been observed to heighten the risk of cardiovascular disease in US adults, particularly in the case of PBB153. Further investigation is warranted through a large-scale cohort study to validate and strengthen these findings.

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Section: Discussionmentioning

confidence: 99%

Single and combined association between brominated flame retardants and cardiovascular disease: a large-scale cross-sectional study

Yin,

Xu,

Zou

et al. 2024

Front. Public Health

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“…On the other hand, glucose works as a flexible substrate as it provides ATP by cytoplasmic glycolysis and mitochondrial oxidation of the pyruvate derived from glucose metabolism. More importantly, glucose supplies ATP most efficiently in the ischemic and stressed myocardium ( Tian et al, 2023 ). Glucose metabolism generates pyruvate, lactate, and acetyl-CoA, which are further used in the pentose phosphate pathway or replenish TCA cycle intermediates in the mitochondria.…”

Section: Metabolic Regulation Of Cardiac Homeostasismentioning

confidence: 99%

Cardiac fibrogenesis: an immuno-metabolic perspective

Hoque,

Gbadegoye,

Hassan

et al. 2024

Front. Physiol.

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Cardiac fibrosis is a major and complex pathophysiological process that ultimately culminates in cardiac dysfunction and heart failure. This phenomenon includes not only the replacement of the damaged tissue by a fibrotic scar produced by activated fibroblasts/myofibroblasts but also a spatiotemporal alteration of the structural, biochemical, and biomechanical parameters in the ventricular wall, eliciting a reactive remodeling process. Though mechanical stress, post-infarct homeostatic imbalances, and neurohormonal activation are classically attributed to cardiac fibrosis, emerging evidence that supports the roles of immune system modulation, inflammation, and metabolic dysregulation in the initiation and progression of cardiac fibrogenesis has been reported. Adaptive changes, immune cell phenoconversions, and metabolic shifts in the cardiac nonmyocyte population provide initial protection, but persistent altered metabolic demand eventually contributes to adverse remodeling of the heart. Altered energy metabolism, mitochondrial dysfunction, various immune cells, immune mediators, and cross-talks between the immune cells and cardiomyocytes play crucial roles in orchestrating the transdifferentiation of fibroblasts and ensuing fibrotic remodeling of the heart. Manipulation of the metabolic plasticity, fibroblast–myofibroblast transition, and modulation of the immune response may hold promise for favorably modulating the fibrotic response following different cardiovascular pathological processes. Although the immunologic and metabolic perspectives of fibrosis in the heart are being reported in the literature, they lack a comprehensive sketch bridging these two arenas and illustrating the synchrony between them. This review aims to provide a comprehensive overview of the intricate relationship between different cardiac immune cells and metabolic pathways as well as summarizes the current understanding of the involvement of immune–metabolic pathways in cardiac fibrosis and attempts to identify some of the previously unaddressed questions that require further investigation. Moreover, the potential therapeutic strategies and emerging pharmacological interventions, including immune and metabolic modulators, that show promise in preventing or attenuating cardiac fibrosis and restoring cardiac function will be discussed.

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“…Glucose and fatty acids are essential substrates for oxidative phosphorylation. Glucose and lipid metabolism plays an important role in cardiac myocytes by providing energy and maintaining cellular function (H. Tian et al, 2023 ). However, studies in murine models of EHS have revealed that HS alters cardiomyocyte metabolic pathways, disrupts the glycolytic and oxidative phosphorylation pathways by upregulating glycolysis-related enzymes, thereby enhancing lactate production to impair cardiomyocyte function ( Laitano et al, 2020 ).…”

Section: The Related Mechanisms Of Hs-induced Myocardial Injurymentioning

confidence: 99%

The pathogenesis and therapeutic strategies of heat stroke-induced myocardial injury

Xia,

Sun,

et al. 2024

Front. Pharmacol.

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Heat stroke (HS) is a febrile illness characterized by an elevation in the core body temperature to over 40°C, accompanied by central nervous system impairment and subsequent multi-organ dysfunction syndrome. In recent years, the mortality rate from HS has been increasing as ambient temperatures continue to rise each year. The cardiovascular system plays an important role in the pathogenesis process of HS, as it functions as one of the key system for thermoregulation and its stability is associated with the severity of HS. Systemic inflammatory response and endothelial cell damage constitute pivotal attributes of HS, other factors such as ferroptosis, disturbances in myocardial metabolism and heat shock protein dysregulation are also involved in the damage to myocardial tissue in HS. In this review, a comprehensively detailed description of the pathogenesis of HS-induced myocardial injury is provided. The current treatment strategies and the promising therapeutic targets for HS are also discussed.

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Abnormalities of glucose and lipid metabolism in myocardial ischemia-reperfusion injury

Cited by 23 publications

References 140 publications

Single and combined association between brominated flame retardants and cardiovascular disease: a large-scale cross-sectional study

Single and combined association between brominated flame retardants and cardiovascular disease: a large-scale cross-sectional study

Cardiac fibrogenesis: an immuno-metabolic perspective

The pathogenesis and therapeutic strategies of heat stroke-induced myocardial injury

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