Mitochondria, essential organelles orchestrating cellular metabolism, have emerged as central players in various disease pathologies. Recent research has shed light on mitohormesis, a concept proposing an adaptive response of mitochondria to minor disturbances in homeostasis, offering novel therapeutic avenues for mitochondria-related diseases. This comprehensive review explores the concept of mitohormesis, elucidating its induction mechanisms and occurrence. Intracellular molecules like reactive oxygen species (ROS), calcium, mitochondrial unfolded proteins (UPRmt), and integrated stress response (ISR), along with external factors such as hydrogen sulfide (HS), physical stimuli, and exercise, play pivotal roles in regulating mitohormesis. Based on the available evidence, we elucidate how mitohormesis maintains mitochondrial homeostasis through mechanisms like mitochondrial quality control and mitophagy. Furthermore, the regulatory role of mitohormesis in mitochondria-related diseases is discussed. By envisioning future applications, this review underscores the significance of mitohormesis as a potential therapeutic target, paving the way for innovative interventions in disease management.
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http://dx.doi.org/10.3390/biology13060394 | DOI Listing |
Biol Direct
January 2025
Key Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu, China.
Background: Despite the increasing body of evidence that mitochondrial activities implicate in chronic obstructive pulmonary disease (COPD), we are still far from a causal-logical and mechanistic understanding of the mitochondrial malfunctions in COPD pathogenesis.
Results: Differential expression genes (DEGs) from six publicly available bulk human lung tissue transcriptomic datasets of COPD patients were intersected with the known mitochondria-related genes from MitoCarta3.0 to obtain mitochondria-related DEGs associated with COPD (MitoDEGs).
Signal Transduct Target Ther
January 2025
Department of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Mitochondria are essential for cellular function and viability, serving as central hubs of metabolism and signaling. They possess various metabolic and quality control mechanisms crucial for maintaining normal cellular activities. Mitochondrial genetic disorders can arise from a wide range of mutations in either mitochondrial or nuclear DNA, which encode mitochondrial proteins or other contents.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopedic Surgery at the First Affiliated Hospital, Harbin Medical University, Harbin, China.
Osteoporosis (OP) is a prevalent age-related bone metabolic disease. Aging and mitochondrial dysfunction are involved in the onset and progression of OP, but the specific mechanisms have not been elucidated. The aim of this study was to identify novel potential biomarkers associated with aging and mitochondria in OP.
View Article and Find Full Text PDFCurr Alzheimer Res
December 2024
Neck-Pain Hospital of Shoulder and Lumbocrural Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Unlabelled:
Introduction: Alzheimer's disease (AD) represents the most common neurodegenerative disorder, characterized by progressive cognitive decline and memory loss. Despite the recognition of mitochondrial dysfunction as a critical factor in the pathogenesis of AD, the specific molecular mechanisms remain largely undefined.
Method: This study aimed to identify novel biomarkers and therapeutic strategies associated with mitochondrial dysfunction in AD by employing bioinformatics combined with machine learning methodologies.
Sci Rep
January 2025
Geriatric Center, Affiliated Hospital of Inner Mongolia Medical University, No.1 Tongdao North Street, Huimin District, Hohhot, 010050, China.
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