Mitophagy in metabolic syndrome

Miao, Mei-Qi; Han, Yubo; Liu, Li

doi:10.1111/jch.14650

Cited by 7 publications

(4 citation statements)

References 56 publications

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“…Correct functioning of cellular mitochondria depends on the selective degradation of impaired ones through autophagy -a process, called mitophagy. Mitophagy impairments are an important part of MS genesis and progression and its corresponding conditions, including cardiovascular implications [16]. Polyphenol-mediated mitophagy presents an opportunity for modulation of mitochondrial health through dietary manipulation [17].…”

Section: Discussionmentioning

confidence: 99%

Japanese Quince Fruit Juice Exerts a Cardioprotective Effect in a Model of Diet-Induced Metabolic Syndrome in Rats

Moneva-Marinova,

Tzaneva,

Gasanzadeeva

et al. 2023

Journal of Biomedical and Clinical Research

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Summary The current study aimed to evaluate the influence of Japanese quince (Chaenomeles japonica) fruit juice (JQFJ) on the myocardium and on the coronary arteries of rats with diet-induced metabolic syndrome (MS). Male Wistar rats (n=50) were divided into 5 groups: Control, MS, MS+JQFJ2.5, MS+JQFJ5 and MS+JQFJ10. MS was induced with a high-fat high-fructose diet for 10 weeks. During that period, all animals were daily orally treated with distilled water (Control and MS groups) or with JQFJ at doses of 2.5 ml/kg, 5 ml/kg and 10 ml/kg (the other three groups, respectively). At the end of the experiment, the myocardium and coronary arteries were examined histopathologically. In group MS, necrotic endothelial cells and exposed basal membrane were observed. JQFJ at 2.5 ml/kg reduced the impairment but activated endothelial cells were still found. JQFJ at 5 ml/kg and 10 ml/kg prevented coronary artery endothelium damage, preserving the normal morphology. The myocardium in MS group presented with cardiomyocyte degeneration and increased distance between the cells. In group MS+JQFJ2.5, the degeneration was decreased. In groups MS+JQFJ5 and MS+JQFJ10, the histology of the myocardium resembled that of the control group. In the current histopathological evaluation, JQFJ prevented the MS-induced impairment of myocardium and coronary arteries.

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Section: Discussionmentioning

confidence: 99%

Japanese Quince Fruit Juice Exerts a Cardioprotective Effect in a Model of Diet-Induced Metabolic Syndrome in Rats

Moneva-Marinova,

Tzaneva,

Gasanzadeeva

et al. 2023

Journal of Biomedical and Clinical Research

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“…The key mitophagy pathways (Figure 1) are divided into receptor-mediated mitophagy and ubiquitin-mediated mitophagy [93,94]. During receptor-mediated mitophagy, under mitochondrial stress (i.e., hypoxia or depolarizing agents), mitophagy receptors localize to the outer mitochondrial membrane.…”

Section: Mitophagy and Mitochondrial Biogenesismentioning

confidence: 99%

Therapeutic Effects of Mesenchymal Stromal Cells Require Mitochondrial Transfer and Quality Control

Mukkala,

Jerkic,

Khan

et al. 2023

IJMS

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Due to their beneficial effects in an array of diseases, Mesenchymal Stromal Cells (MSCs) have been the focus of intense preclinical research and clinical implementation for decades. MSCs have multilineage differentiation capacity, support hematopoiesis, secrete pro-regenerative factors and exert immunoregulatory functions promoting homeostasis and the resolution of injury/inflammation. The main effects of MSCs include modulation of immune cells (macrophages, neutrophils, and lymphocytes), secretion of antimicrobial peptides, and transfer of mitochondria (Mt) to injured cells. These actions can be enhanced by priming (i.e., licensing) MSCs prior to exposure to deleterious microenvironments. Preclinical evidence suggests that MSCs can exert therapeutic effects in a variety of pathological states, including cardiac, respiratory, hepatic, renal, and neurological diseases. One of the key emerging beneficial actions of MSCs is the improvement of mitochondrial functions in the injured tissues by enhancing mitochondrial quality control (MQC). Recent advances in the understanding of cellular MQC, including mitochondrial biogenesis, mitophagy, fission, and fusion, helped uncover how MSCs enhance these processes. Specifically, MSCs have been suggested to regulate peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC1α)-dependent biogenesis, Parkin-dependent mitophagy, and Mitofusins (Mfn1/2) or Dynamin Related Protein-1 (Drp1)-mediated fission/fusion. In addition, previous studies also verified mitochondrial transfer from MSCs through tunneling nanotubes and via microvesicular transport. Combined, these effects improve mitochondrial functions, thereby contributing to the resolution of injury and inflammation. Thus, uncovering how MSCs affect MQC opens new therapeutic avenues for organ injury, and the transplantation of MSC-derived mitochondria to injured tissues might represent an attractive new therapeutic approach.

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“…Consequently, recent findings underscore the significance of mitophagy—the process that selectively eliminates damaged mitochondria from cells, facilitating their degradation by lysosomes and maintaining mitochondrial homeostasis—in the pathophysiology of Metabolic Syndrome (MetS). There is a suggestion for its potential therapeutic application in the future [ 79 ].…”

Section: A Correlation Exists: But Why?mentioning

confidence: 99%

Metabolic Syndrome and Atrial Fibrillation: Different Entities or Combined Disorders

Zakynthinos,

Tsolaki,

Oikonomou

et al. 2023

JPM

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Obesity, hypertension, insulin resistance, and dyslipidemia are all clusters of an entity called “Metabolic Syndrome”. The global trends of this syndrome’s incidence/prevalence continue to increase reciprocally, converting it into a massive epidemic problem in the medical community. Observing the risk factors of atrial fibrillation, a medical condition that is also converted to a scourge, almost all parts of the metabolic syndrome are encountered. In addition, several studies demonstrated a robust correlation between metabolic syndrome and the occurrence of atrial fibrillation. For atrial fibrillation to develop, a combination of the appropriate substrate and a trigger point is necessary. The metabolic syndrome affects the left atrium in a multifactorial way, leading to atrial remodeling, thus providing both the substrate and provoking the trigger needed, which possibly plays a substantial role in the progression of atrial fibrillation. Due to the remodeling, treatment of atrial fibrillation may culminate in pernicious sequelae, such as repeated catheter ablation procedures. A holistic approach of the patient, with simultaneous treatment of both entities, is suggested in order to ensure better outcomes for the patients.

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Mitophagy in metabolic syndrome

Cited by 7 publications

References 56 publications

Japanese Quince Fruit Juice Exerts a Cardioprotective Effect in a Model of Diet-Induced Metabolic Syndrome in Rats

Japanese Quince Fruit Juice Exerts a Cardioprotective Effect in a Model of Diet-Induced Metabolic Syndrome in Rats

Therapeutic Effects of Mesenchymal Stromal Cells Require Mitochondrial Transfer and Quality Control

Metabolic Syndrome and Atrial Fibrillation: Different Entities or Combined Disorders

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