Sep 2026· Chinese Journal of Natural Medicines· Vol 24 9, pp.
1068-1080
· 0 citations· 193 references
Medicine
TL;DR
This review systematically summarize the specific mitochondrial pathological phenotypes in various diseases and provides a comprehensive overview of natural products that correspond to these phenotypes, along with their mechanisms of action.
Abstract
Mitochondria are indispensable organelles that serve as the powerhouses of cells, playing a crucial role in maintaining cellular energy homeostasis. Consequently, mitochondrial dysfunction is recognized as a key pathogenic factor in a wide range of common diseases, including cardiovascular diseases, neurodegenerative disorders, metabolic syndromes and cancers. Due to their multitarget properties and favorable safety profiles, natural products have shown significant potential for regulating key mitochondrial biological processes, including mitobiogenesis, mitophagy, mitochondrial dynamics (fusion and fission), oxidative phosphorylation, and mitochondria-mediated apoptosis. Therefore, they have become an important resource for mitochondria-targeted therapy. Despite significant progress in mechanistic studies in vitro, translating these findings into clinical applications remains a major challenge. This translational gap is primarily due to unfavorable pharmaceutical properties, such as low bioavailability, poor targeted delivery, and rapid metabolic clearance. Additionally, the precise mechanisms governing mitochondria remain to be fully elucidated. In this review, we systematically summarize the specific mitochondrial pathological phenotypes in various diseases and provide a comprehensive overview of natural products that correspond to these phenotypes, along with their mechanisms of action. We also analyze common challenges associated with the absorption, distribution, metabolism, and excretion of these products. By bridging the gap between basic research and clinical application, this review aims to accelerate the development of novel therapeutic strategies for mitochondria-related diseases.
Recent studies demonstrate promising therapeutic targets for mitochondrial dysfunction and highlight the need for research in mitochondrial function to change the therapeutic landscape in the management of mitochondrial dysfunction-associated diseases.
Olufemi Akintayo Akinkunmi, Feyikemi Funmilayo Araba, J. A. Chukwudebelu et al.· Frontiers in Cell and Develo...· 0 citations
Highlights What are the main findings? Macroautophagy and its selective forms play an important, multifaceted and often bidirectional role in the pathogenesis of mitochondrial diseases. The role of autophagy in cellular organelles, apart from mitophagy, has not been sufficiently investigated. What are the implications of the main findings? Restoring autophagy improves mitochondrial function and cell survival in mitochondrial disorders. Studying autophagy in cellular organelles, apart from mitochondria, has the potential to reveal new mechanisms underlying the cellular pathogenesis of mitochondrial diseases and to find new promising approaches to treatment. Abstract Mitochondrial diseases are a heterogeneous group of inherited disorders caused by defects in the mitochondrial genome or nuclear genes encoding proteins essential for mitochondrial function. These conditions are characterised by progressive dysfunction of tissues with high energy demands, particularly the nervous and muscular systems. In recent years, increasing consideration has been paid to the role of autophagy—the cellular mechanism for the degradation and recycling of intracellular components in the pathogenesis of mitochondrial diseases. This review synthesizes current knowledge on molecular mechanisms of macroautophagy and selective forms of au-tophagy targeting specific organelles and structures: mitophagy, pexophagy, ribophagy, ER-phagy, aggrephagy, lipophagy, lisophagy, and nucleophagy. Using classic mitochondrial syndromes—Kearns–Sayre syndrome (KSS), MERRF, and MELAS, as well as various mitochondrial myopathies—as examples, we discuss experimental evidence indicating both compensatory activation of autophagy and its insufficiency or blockade at different stages. Furthermore, we examine the link between deficiencies of key fatty acid β-oxidation enzymes (VLCAD, MCAD, CPT2) and impaired autophagic flux, including secondary defects of mitophagy mediated by energy deficiency. The review systematises current understanding of how dysregulation of selective autophagy promotes the accumulation of damaged mitochondria, oxidative stress, inflammation, and cell death in mitochondrial diseases. Prospects for therapeutic modulation of autophagy as a potential approach to treating these disorders are discussed.
E. D. Avdonina, Sergey I Kutsev, A. Shestopalov· Cells· 0 citations
The different facets of mitochondrial quality control are explored and their implications in disease progression and aging are discussed, providing an overview of their potential to mitigate disease burden and promote healthy aging.
Agustina Creus, Shrestha Mohapatra, Leonardo Ortega et al.· Signal Transduction and Targ...· 1 citation
Simple Summary As we age, our bodies gather senescent cells that evade apoptosis and release detrimental signals, resulting in systemic inflammation and conditions such as dementia and heart failure. A significant contributor to their detrimental effects is the decline in mitochondrial function, which leads to the leakage of harmful substances and inflammatory reactions. Natural compounds derived from fruits, vegetables, and herbs have the potential to restore mitochondrial function and eliminate these senescent cells. Nevertheless, a significant obstacle is that these compounds seldom reach the mitochondria upon ingestion. This review explores micro-delivery systems that are designed to transport natural compounds directly to the mitochondria. Our findings indicate that both the natural repair compounds and delivery technologies exist, but surprisingly, no studies have yet combined them to target aging cells. We suggest the integration of these strategies to create innovative therapies that could decelerate the aging process and tackle various age-related diseases.
Jirapat Namkaew, P. Kongpracha, Thiranut Jaroonwitchawan· Biology· 0 citations
This review focuses on the core mechanisms that link mitochondrial dysfunction to disease progression and the major barriers to translation, and examines biomarker development and the major barriers to translation.
L. Elabbasy· Current opinion in pharmacol...· 0 citations
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