Mitochondrial dysfunction is increasingly recognized as a central contributor to the pathogenesis of cardiovascular diseases (CVDs), including heart failure, ischemic heart disease, hypertension, and cardiomyopathy. Mitochondria, known as the powerhouses of the cell, play a vital role in maintaining cardiac energy homeostasis, regulating reactive oxygen species (ROS) production and controlling cell death pathways. Dysregulated mitochondrial function results in impaired adenosine triphosphate (ATP) production, excessive ROS generation, and activation of apoptotic and necrotic pathways, collectively driving the progression of CVDs. This review provides a detailed examination of the molecular mechanisms underlying mitochondrial dysfunction in CVDs, including mutations in mitochondrial DNA (mtDNA), defects in oxidative phosphorylation (OXPHOS), and alterations in mitochondrial dynamics (fusion, fission, and mitophagy). Additionally, the role of mitochondrial dysfunction in specific cardiovascular conditions is explored, highlighting its impact on endothelial dysfunction, myocardial remodeling, and arrhythmias. Emerging therapeutic strategies targeting mitochondrial dysfunction, such as mitochondrial antioxidants, metabolic modulators, and gene therapy, are also discussed. By synthesizing recent advances in mitochondrial biology and cardiovascular research, this review aims to enhance understanding of the role of mitochondria in CVDs and identify potential therapeutic targets to improve cardiovascular outcomes.
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http://dx.doi.org/10.3390/ijms26051917 | DOI Listing |
Clin Ther
March 2025
Fondazione IRCCS Istituto Neurologico Carlo Besta, Medical Genetics and Neurogenetics Unit, Milan, Italy. Electronic address:
Purpose: The 6 months pilot, single arm, phase I/II, open-label clinical trial PHEMI investigated the safety and efficacy of daily administration of phenylbutyrate in reducing lactic acidosis by at least 20% in 3 children (ages 7-10 yrs) with pyruvate dehydrogenase deficiency and 6 adults with mitochondrial myopathy encephalopathy lactic acidosis and stroke-like episodes. As a side study, we investigated the response to phenylbutyrate treatment in skin fibroblasts and cybrids derived from PHEMI patients with the aim of unraveling a possible in vivo-in vitro correlation.
Methods: Safety was assessed through the collection of vital signs, clinical evaluations, blood samples, and reported adverse events.
BMJ Open Ophthalmol
March 2025
Department of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, Stockholm, Sweden
Background: Glaucoma, a leading cause of irreversible blindness worldwide, is characterised by retinal ganglion cell degeneration. Increasing evidence points to metabolic dysfunction, particularly mitochondrial dysfunction, as a contributing factor to glaucomatous neurodegeneration. This systematic review and meta-analysis aimed to identify key metabolic pathways and biomarkers associated with primary open-angle glaucoma (POAG).
View Article and Find Full Text PDFJ Biol Chem
March 2025
Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, 100 Haike Road, Pudong New District, Shanghai, 201210, China. Electronic address:
Pathological stress can lead to failure in the translocation of mitochondrial proteins, resulting in accumulation of unimported proteins within the cytosol and upregulation of proteasome for their quality control. Malfunction or delay in protein clearance causes dysregulation of mitochondrial protein homeostasis, cellular toxicity, and diseases. Ubiquilins (UBQLNs) are known to serve as chaperone which associates with unimported mitochondrial membrane protein precursors, and facilitates their proteasomal degradation.
View Article and Find Full Text PDFChem Biol Interact
March 2025
Department of Environmental Science, Baylor University, Waco, TX 76798. Electronic address:
Bisphenol analogs, structurally similar to bisphenol A (BPA), are widely used in various industries as a safer alternative to BPA. However, these alternatives also present risks, such as inflammation and potential connections to chronic diseases like cancer and diabetes, highlighting the need for further research into their toxicity mechanisms. Building on our previous cytotoxicity research, this study delves into the mechanisms of toxicity associated with bisphenol analogs (bisphenol AF, bisphenol AP, bisphenol E, and bisphenol P) on human in vitro cell models (HepaRG, Caco-2, HMC3, and HMEC-1).
View Article and Find Full Text PDFChem Biol Interact
March 2025
Yichun People's Hospital, Yichun, Jiangxi Province, China. Electronic address:
Environmental pollution is a significant contributor to male infertility. Numerous environmental pollutants, such as PCB118, act as exogenous ligands for the aryl hydrocarbon receptor (AhR). However, the role of AhR in mediating the effects of environmental pollutants on male reproductive functions remains inadequately understood.
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