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Mitochondria in Aging and Aging-Related Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 May 2025) | Viewed by 1305

Special Issue Editor

Special Issue Information

Dear Colleagues,

Aging is a chronic functional disarrangement and is the dominant risk factor for most human diseases. Mitochondria are a central hub of aging. Alterations in mitochondrial morphology and decline in mitochondrial function have been widely observed during aging, manifested by elevated ROS production, mitochondrial DNA (mtDNA) mutations, protein oxidation and abnormal energy metabolism, changes in mitochondrial content and mitochondrial biogenesis. As a consequence, these structural and functional defects in mitochondria impaired mitochondrial quality control, mitochondrial dynamics, and mitochondrial-to-nuclear signalling, all of which result in cellular senescence and a variety of aging-related pathophysiological characteristics. For instance, mitochondria are functionally required in high-energy demanding tissues like the heart, skeletal muscle, and brain. Therefore, aging-related mitochondrial dysfunction and subsequent abnormal cell signalling have been observed in many diseases affecting these tissues, including cardiomyopathy, atherosclerosis, hypertension, aortic aneurysm, aortic dissection, Parkinson’s disease (PD), and Alzheimer’s disease (AD). In addition, the aging-related accumulation of mtDNA mutations causes metabolic remodelling, genomic instability and inflammation, and contributes to carcinogenesis, Marfan syndrome, Werner syndrome, and ataxia telangiectasia with unclear cellular and molecular mechanisms.

Contributions to this Special Issue will further explore the fields of mitochondria in aging and aging-related diseases and provide a theoretical and molecular basis for developing new strategies for human health and treating related diseases. Well-designed research articles and reviews on these related topics, especially at the cellular and molecular levels, are welcome.

Dr. Yongting Luo
Guest Editor

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Keywords

  • mitochondria
  • aging
  • reactive oxygen species
  • antioxidants
  • mitochondrial metabolism
  • mitochondrial biogenesis
  • mitochondrial dynamics
  • mtDNA mutations
  • mitophagy
  • mitochondrial signalling
  • inflammation
  • cancer
  • metabolic disease
  • cardiovascular disease
  • neurodegenerative disease
  • life span

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Published Papers (1 paper)

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Review

34 pages, 2865 KB  
Review
Mitochondrial Transport Proteins in Cardiovascular Diseases: Metabolic Gatekeepers, Pathogenic Mediators and Therapeutic Targets
by Yue Pei, Sitong Wan, Jingyi Qi, Xueyao Xi, Yinhua Zhu, Peng An, Junjie Luo and Yongting Luo
Int. J. Mol. Sci. 2025, 26(17), 8475; https://doi.org/10.3390/ijms26178475 - 31 Aug 2025
Viewed by 718
Abstract
Mitochondria, as the metabolic hubs of cells, play a pivotal role in maintaining cardiovascular homeostasis through dynamic regulation of energy metabolism, redox balance, and calcium signaling. Cardiovascular diseases (CVDs), including heart failure, ischemic heart disease, cardiomyopathies, and myocardial infarction, remain the leading cause [...] Read more.
Mitochondria, as the metabolic hubs of cells, play a pivotal role in maintaining cardiovascular homeostasis through dynamic regulation of energy metabolism, redox balance, and calcium signaling. Cardiovascular diseases (CVDs), including heart failure, ischemic heart disease, cardiomyopathies, and myocardial infarction, remain the leading cause of global mortality, with mitochondrial dysfunction emerging as a unifying pathological mechanism across these conditions. Emerging evidence suggests that impaired mitochondrial transport systems—critical gatekeepers of metabolite flux, ion exchange, and organelle communication—drive disease progression by disrupting bioenergetic efficiency and exacerbating oxidative stress. This review synthesizes current knowledge on mitochondrial transport proteins, such as the voltage-dependent anion channels, transient receptor potential channels, mitochondrial calcium uniporter, and adenine nucleotide translocator, focusing on their structural–functional relationships and dysregulation in CVD pathogenesis. We highlight how aberrant activity of these transporters contributes to hallmark features of cardiac pathology, including metabolic inflexibility, mitochondrial permeability transition pore destabilization, and programmed cell death. Furthermore, we critically evaluate preclinical advances in targeting mitochondrial transport systems through pharmacological modulation, gene editing, and nanoparticle-based delivery strategies. By elucidating the mechanistic interplay between transport protein dysfunction and cardiac metabolic reprogramming, we address a critical knowledge gap in cardiovascular biology and provide a roadmap for developing precision therapies. Our insights underscore the translational potential of mitochondrial transport machinery as both diagnostic biomarkers and therapeutic targets, offering new avenues to combat the growing burden of CVDs in aging populations. Full article
(This article belongs to the Special Issue Mitochondria in Aging and Aging-Related Diseases)
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