Mitochondrial function, dynamics and quality control in the pathophysiology of HFpEF

Campo, Andrea del; Pérez, Gonzalo; Castro, Pablo; Parra, Valentina; Verdejo, Hugo

doi:10.1016/j.bbadis.2021.166208

Cited by 20 publications

(13 citation statements)

References 196 publications

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“…The mechanisms underlying mitomiRs biogenesis and action sites are still poorly understood, however they are a fascinating class of miRNAs which could allow to track the mitochondrial status and health in pathological conditions (Latronico and Condorelli, 2012). Indeed, differentially expressed mitomiRs have been observed in heart failure (Pinti et al, 2017;Wang et al, 2017), where mitochondrial dysfunction is evident (Santulli et al, 2015;Sties et al, 2018;Del Campo et al, 2021;Guitart-Mampel et al, 2021;Morciano et al, 2021;Yang et al, 2021;Schwemmlein et al, 2022). Despite their potential power in mirroring systemic mitochondrial homeostasis, the assessment of mitomiRs in FD has never been contemplated.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial microRNAs Are Dysregulated in Patients with Fabry Disease

Gambardella

Fiordelisi

Sorriento

et al. 2022

J Pharmacol Exp Ther

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We demonstrate for the first time that a specific signature of circulating mitochondrial microRNAs (mitomiRs) is dysregulated in Fabry disease (FD). In our study, we observed that mitomiRs regulating fundamental aspects of mitochondrial homeostasis and fitness, including expression and assembly of the respiratory chain, mitogenesis, antioxidant capacity, and apoptosis are significantly dysregulated in FD patients. Taken together, our new findings introduce mitomiRs as unprecedented biomarkers of FD and point at mitochondrial dysfunction as a novel potential mechanistic target for therapeutic approaches.

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Section: Introductionmentioning

confidence: 99%

Mitochondrial microRNAs Are Dysregulated in Patients with Fabry Disease

Gambardella

Fiordelisi

Sorriento

et al. 2022

J Pharmacol Exp Ther

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“…Mitochondria is the most important organelle involved in cellular or tissue metabolic physiological processes [ 5 ]. Since mitochondrial homeostasis is vital to maintaining physical cellular activity, mitochondrial quality control disorders through various processes such as proteostasis, mitochondrial dynamics, and mitophagy could lead to the development of metabolic syndrome–related cardiomyopathy (MSC) [ 6 ]. In this review, we would first introduce the changes in MSC, and then we will review the role of dysregulated mitochondrial homeostasis in cardiomyopathy induced by metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

The Role of Mitochondria in Metabolic Syndrome–Associated Cardiomyopathy

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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With the rapid development of society, the incidence of metabolic syndrome (MS) is increasing rapidly. Evidence indicated that patients diagnosed with MS usually suffered from cardiomyopathy, called metabolic syndrome–associated cardiomyopathy (MSC). The clinical characteristics of MSC included cardiac hypertrophy and diastolic dysfunction, followed by heart failure. Despite many studies on this topic, the detailed mechanisms are not clear yet. As the center of cellular metabolism, mitochondria are crucial for maintaining heart function, while mitochondria dysfunction plays a vital role through mechanisms such as mitochondrial energy deprivation, calcium disorder, and ROS (reactive oxygen species) imbalance during the development of MSC. Accordingly, in this review, we will summarize the characteristics of MSC and especially focus on the mechanisms related to mitochondria. In addition, we will update new therapeutic strategies in this field.

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“…Furthermore, anomalies in the oxidative stress system have been linked to endoplasmic reticulum stress. High-level oxidative stress in the endoplasmic reticulum harasses the healthy functioning of cells, causing various heart diseases such as cardiac hypertrophy, myocardial infarction, cardiac insufficiency, and heart failure [ 3 , 6 ]. The extensive clinical and animal experiments have expounded that OSA induces an increase in the ratio of heart weight : body weight (HW : BW) and enhances the levels of plasma atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and angiotensin II (An g II) [ 7 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

Silencing MR-1 Protects against Myocardial Injury Induced by Chronic Intermittent Hypoxia by Targeting Nrf2 through Antioxidant Stress and Anti-Inflammation Pathways

Wang

Zhang

et al. 2022

Journal of Healthcare Engineering

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Background. Patients with obstructive sleep apnea hypopnea syndrome (OSAHS) often have cardiac insufficiency mainly due to hypoxia/reperfusion injury caused by chronic intermittent hypoxia (CIH). Inflammation and oxidative stress are involved in the cardiovascular events of OSAHS patients. Studies have found that myofibrillation regulator-1 (MR-1) participates in the pathological process of OSAHS-induced myocardial injury, but the specific mechanism is still unclear. Methods. We used a CIH-induced rat model to simulate the process of OSAHS disease. Indices of myocardial injury, inflammation, and oxidative stress were detected using quantitative PCR and enzyme-linked immunosorbent assay (ELISA). After administration of adenoassociated viral vector (AAV) encoding silencing RNA against MR-1, we examined expression of the classic antioxidant stress pathway protein NF-E2-related factor 2 (Nrf2) using western blotting. Results. We found that levels of serum inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 were increased, and we further observed disturbance of the oxidative stress system, in which the content of reactive oxygen species (ROS), superoxide dismutase (SOD), reduced glutathione (GSH), and malondialdehyde (MDA) was enhanced in CIH-induced rats. Subsequently, we detected that expression of Nrf2 and heme oxygenase-1 (HO-1) was slightly increased, while the expression of Kelch-like ECH-associated protein 1 (Keap-1) was significantly increased in the CIH model. Interestingly, after administration of silencing MR-1 AAV, the elevated levels of inflammatory factors were reduced, and the disordered oxidative stress system was corrected. Additionally, the expression of Nrf2 and HO-1 was distinctly increased, but the high expression of Keap-1 was decreased. Conclusions. Our research results demonstrate that silencing MR-1 rescued the myocardium the injury from inflammatory and oxidative stress in CIH-induced rats by administration of the Nrf2 signaling pathway.

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Mitochondrial function, dynamics and quality control in the pathophysiology of HFpEF

Cited by 20 publications

References 196 publications

Mitochondrial microRNAs Are Dysregulated in Patients with Fabry Disease

Mitochondrial microRNAs Are Dysregulated in Patients with Fabry Disease

The Role of Mitochondria in Metabolic Syndrome–Associated Cardiomyopathy

Silencing MR-1 Protects against Myocardial Injury Induced by Chronic Intermittent Hypoxia by Targeting Nrf2 through Antioxidant Stress and Anti-Inflammation Pathways

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