Aug 2026· Frontiers in Cell and Developmental Biology· Vol 14· 0 citations· 157 references
Medicine
TL;DR
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.
Abstract
Although the mitochondria are known as the cellular powerhouse, their function is beyond energy generation. These organelles regulate cellular metabolism, yet maintains a tightly regulated reactive oxygen species (ROS) generation and optimal redox state. In addition, mitochondria serve as mediators of physiological and pathological processes, such as maintenance of calcium balance, and control of apoptosis and mitophagy. All these make the mitochondria a major factor in both cellular and organismal regulation. However, mitochondria dysfunction may occur through many processes, including genetic mutations, increased production of ROS, metabolic failure from impaired electron transport chain activity, and dysregulated dynamics or mitophagy. Several self-perpetuating damages accumulate from these processes and influence clinical pathologies, such as aging, metabolic syndrome, cancer, neurodegeneration, and reproductive disorders. Recent studies demonstrate promising therapeutic targets for mitochondrial dysfunction. Examples include targeted antioxidants, such as MitoQ and SkQ1, to selectively neutralize mitochondrial ROS, pharmacological modulators to enhance mitochondrial biogenesis and to restore NAD+ homeostasis via PGC-1α activation, gene-editing technologies, such as mitoTALENs and mtZFNs to selectively eliminate pathogenic mitochondrial DNA mutations, and mitochondrial transplantation as a new technique to replace damaged organelles. Together, these novel approaches highlight the need for research in mitochondrial function to change the therapeutic landscape in the management of mitochondrial dysfunction-associated diseases.
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.
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Mitochondria, often referred to as the powerhouses of the cell, play a pivotal role in maintaining cellular homeostasis through the regulation of energy production, redox balance, and apoptosis. Recent evidence highlights the significance of mitochondrial dynamics, fusion, fission, biogenesis, and mitophagy, enabling cells to adapt to changing physiological and environmental conditions. Dysregulation of these dynamic processes alters mitochondrial function, promoting metabolic reprogramming, evasion of apoptosis, and resistance to chemotherapy. Specifically, enhanced mitochondrial fission is often linked to increased metabolic flexibility and resistance to cell death, while aberrant fusion supports mitochondrial quality control under cellular stress. Additionally, tumour cells also exhibit bioenergetic flexibility, dynamically switching between OXPHOS and glycolysis to meet energy demands and overcome therapeutic stress. This metabolic change influences ROS levels, directly affecting the efficacy of anticancer agents in cancer cells. Such adaptations are now recognised as hallmarks of drug-resistant cancers. This review explores the mechanistic interplay between mitochondrial dynamics and cancer bioenergetics, emphasising how these processes contribute to drug resistance. We also focus on emerging therapeutic strategies, particularly smallmolecule inhibitors targeting mitochondrial fusion and fission that offer promising potential to restore chemosensitivity and disrupt cancer cell survival. A deeper understanding of mitochondrial behaviour in cancer may reveal novel therapeutic targets for the development of more effective and durable cancer treatments.
Varsha Johariya, Vaibhav Singh, Rakesh Kore et al.· Mini-Reviews in Medical Chem...· 0 citations
Mitochondria are central regulators of cellular metabolism and survival and play a pivotal role in cancer development and progression through the production of reactive oxygen species (ROS), control of calcium homeostasis, regulation of autophagy, and modulation of cell death pathways. Mitochondria-derived ROS (mtROS) act as signaling mediators that influence tumor initiation, proliferation, metabolic reprogramming, metastasis, and therapeutic resistance by altering redox homeostasis, damaging mitochondrial DNA, and reshaping the tumor microenvironment. In addition to meeting the bioenergetic and biosynthetic requirements of rapidly proliferating cancer cells, mitochondrial metabolism modulates immune responses and supports cancer cell adaptation to hypoxia and nutrient deprivation. Accumulating evidence also highlights the dual role of mtROS, which can promote tumor progression at moderate levels yet trigger oxidative stress-induced cell death when excessively increased, making mitochondrial redox signaling an attractive therapeutic target. This review summarizes the major sources and regulation of mtROS, their involvement in cancer-associated signaling pathways, mitochondrial calcium dynamics, metabolic adaptations, and resistance to anticancer therapies, and discusses current and emerging mitochondrial-targeted strategies aimed at exploiting mtROS signaling to improve cancer treatment outcomes.
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