bims-mistre Biomed News
on Mito stress
Issue of 2025–04–27
thirteen papers selected by
Ellen Siobhan Mitchell, MitoQ
  1. Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration.
  2. The Potential of Coenzyme Q10 in Alzheimer's Disease: Reducing IL-17 Induced Inflammation and Oxidative Stress for Neuroprotection.
  3. NLRP3 inflammasome in Alzheimer's disease: molecular mechanisms and emerging therapies.
  4. Novel Molecules Targeting Metabolism and Mitochondrial Function in Cardiac Diseases.
  5. S-9-PAHSA Attenuates Aβ Accumulation and Improves Cognitive Deficits by Promoting Mitochondrial Autophagy in 5xFAD Mice.
  6. Mitophagy in Neurons: Mechanisms Regulating Mitochondrial Turnover and Neuronal Homeostasis.
  7. ExermiR-129-3p Enhances Muscle Function by Improving Mitochondrial Activity Through PARP1 Inhibition.
  8. Mitochondrial calpain-1 truncates ATP synthase beta subunit.
  9. The association between serum growth differentiation factor 15 and insulin resistance in women diagnosed with polycystic ovary syndrome.
  10. TOM20-driven E3 ligase recruitment regulates mitochondrial dynamics through PLD6.
  11. Crocin extends lifespan by mitigating oxidative stress and regulating lipid metabolism through the DAF-16/FOXO pathway.
  12. The REDOX balance in the prefrontal cortex is positively modulated by aerobic exercise and altered by overfeeding.
  13. Restoration of mitochondrial energy metabolism by electroconvulsive therapy in adolescent and juvenile mice.
  1. Cell Mol Neurobiol. 2025 Apr 21. 45(1): 38
    Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration.
    Donghui Na, Zechen Zhang, Meng Meng, Meiyu Li, Junyan Gao, Jiming Kong, Guohui Zhang, Ying Guo.
      Aging is characterized by a gradual decline in physiological functions, with brain aging being a major risk factor for numerous neurodegenerative diseases. Given the brain's high energy demands, maintaining an adequate ATP supply is crucial for its proper function. However, with advancing age, mitochondria dysfunction and a deteriorating energy metabolism lead to reduced overall energy production and impaired mitochondrial quality control (MQC). As a result, promoting healthy aging has become a key focus in contemporary research. This review examines the relationship between energy metabolism and brain aging, highlighting the connection between MQC and energy metabolism, and proposes strategies to delay brain aging by targeting energy metabolism.
    Keywords:  Brain aging; Energy metabolism; Mitochondrial quality control; Neurons
    DOI:  https://doi.org/10.1007/s10571-025-01555-z
  2. Curr Drug Res Rev. 2025 Apr 24.
    The Potential of Coenzyme Q10 in Alzheimer's Disease: Reducing IL-17 Induced Inflammation and Oxidative Stress for Neuroprotection.
    Himanshu Sharma, Sumaiya Binte Ibrahim, Abdullah Al Noman, Umme Fathima Tuz Zohora, Farhana Akter Shifa, Samira Siddika, Sadia Tasneem, Md Al Azad, Rashmi Pathak.
      Alzheimer's disease (AD) is a progressive neurodegenerative disorder primarily marked by amyloid-beta (Aβ) plaque accumulation and neurofibrillary tangles, which lead to cognitive decline. Oxidative stress and neuroinflammation are key contributors to the disease's progression, with elevated production of Reactive Oxygen Species (ROS) exacerbating neuronal damage. Coenzyme Q10 (CoQ10), a naturally occurring antioxidant, has been identified for its potential neuroprotective effects due to its roles in mitochondrial function, energy production, and antioxidant defense. The cytokine interleukin-17 (IL-17) is also implicated in AD, promoting neuroinflammation by disrupting the blood-brain barrier (BBB) and activating glial cells. This review explores the impact of CoQ10 on neuroinflammation and oxidative stress in AD, focusing on its role in mitigating IL-17-mediated pathways. Preclinical studies indicate that CoQ10 reduces Aβ plaques, improves cognitive functions, and restores mitochondrial stability. However, clinical trials have yielded mixed results, often limited by bioavailability challenges. This research highlights the necessity of further human trials better to understand CoQ10's therapeutic potential in AD management.
    Keywords:  Alzheimer's disease; coenzyme Q10; interleukin-17.; neuroinflammation; oxidative stress
    DOI:  https://doi.org/10.2174/0125899775373406250411104442
  3. Front Immunol. 2025 ;16 1583886
    NLRP3 inflammasome in Alzheimer's disease: molecular mechanisms and emerging therapies.
    Zhitao Li, Chunrong Gong.
      Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuroinflammation, with no definitive cure currently available. The NLRP3 inflammasome, a key mediator of neuroinflammation, has emerged as a critical player in AD pathogenesis, contributing to the accumulation of β-amyloid (Aβ) plaques, tau hyperphosphorylation, and neuronal damage. This review explores the mechanisms by which the NLRP3 inflammasome is activated in AD, including its interactions with Aβ, tau, reactive oxygen species (ROS), and pyroptosis. Additionally, it highlights the role of the ubiquitin system, ion channels, autophagy, and gut microbiota in regulating NLRP3 activation. Therapeutic strategies targeting the NLRP3 inflammasome, such as IL-1β inhibitors, natural compounds, and novel small molecules, are discussed as promising approaches to mitigate neuroinflammation and slow AD progression. This review underscores the potential of NLRP3 inflammasome inhibition as a therapeutic avenue for AD.
    Keywords:  Alzheimer’s disease; IL-1β; NLRP3; inflammasome; inhibitor; microglia; neuro-inflammation
    DOI:  https://doi.org/10.3389/fimmu.2025.1583886
  4. Curr Cardiol Rev. 2025 Apr 18.
    Novel Molecules Targeting Metabolism and Mitochondrial Function in Cardiac Diseases.
    Samir Bolivar Gonzalez, César Vásquez Trincado, Karen Patricia Torres Rodríguez, Lizeth Paola Forero Acosta, Maria Fernanda Perez García, Steffy Saavedra Castro, Sara Camila Castiblanco Arroyave, Gerardo Manríquez Higuera, Luis Antonio Díaz Ariza, Héctor Rodríguez Ortiz, Evelyn Mendoza-Torres.
      Cardiovascular diseases (CVD) are the leading cause of death worldwide, creating the need for new therapeutic strategies targeting the pathological processes involved. Mitochondria, which comprise one-third of cardiac cell volume, maybe a potential therapeutic target for CVD. Known primarily for energy production, mitochondria are also involved in other processes including intermediary metabolism, mitophagy, calcium homeostasis, and regulation of cell apoptosis. Mitochondrial function is closely linked to morphology, which is altered through mitochondrial dynamics, including processes such as fission and fusion, which ensure that the energy needs of the cell are met. Recent data indicate that mitochondrial dysfunction is involved in the pathophysiology of several CVDs, including cardiac hypertrophy, heart failure, ischemia/reperfusion injury, and cardiac fibrosis. Furthermore, mitochondrial dysfunction is associated with oxidative stress related to atherosclerosis, hypertension, and pulmonary hypertension. In this review, we first briefly present the physiological mechanisms of mitochondrial function in the heart and then summarize the current knowledge on the impact of mitochondrial dysfunction on CVD. And finally, we highlight the evidence from in vitro, in vivo, and clinical studies of the cardioprotective effects of drugs that preserve mitochondrial function in CVD. It is hoped that this review may provide new insights into the need to discover new pharmacological targets with direct actions on mitochondria that may provide combined therapeutic strategies to optimally treat these pathologies.
    Keywords:  Cardiovascular disease; angiotensins; cardiac hypertrophy; heart failure; ischemia; metformin; mitochondrial dynamics; nicotinamide riboside.
    DOI:  https://doi.org/10.2174/011573403X372565250331190001
  5. Eur J Neurosci. 2025 Apr;61(8): e70118
    S-9-PAHSA Attenuates Aβ Accumulation and Improves Cognitive Deficits by Promoting Mitochondrial Autophagy in 5xFAD Mice.
    Chenyu Lu, Jiaoqi Ren, Shanshan Huang, Meng Wang, Houguang Zhou, Jingchun Guo.
      Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by significant cognitive impairment and predominantly affects the elderly. With no effective cure available, research continues to explore novel therapeutic and preventive strategies. Recently, palmitic acid-hydroxystearic acids (PAHSAs), especially their stereochemistry S-configuration, have shown potential as a dietary supplement with anti-inflammatory and anti-diabetic properties. We previously found that one of the PAHSAs, 9-PAHSA, could improve cognitive impairment in the high-fat-diet mice, however, whether it has an equal effect on AD-like mice remains unclear. Since mitochondrial dysfunction is recognized as a significant pathological feature of AD, with impaired mitophagy leading to the accumulation of dysfunctional mitochondria, thus exacerbating disease progression, in this study, we evaluated the effects of the chiral isomer of 9-PAHSA, S-9-PAHSA, on cognitive dysfunction and mitochondrial dysfunction in 5xFAD mice. Three-month-old mice were treated with S-9-PAHSA 30 mg/kg in their drinking water for 3 months. Behavioral studies were conducted using the Morris Water Maze (MWM) and Y-maze tests, followed by assessments of amyloid-beta (Aβ) plaque deposition, neuronal apoptosis, and mitochondrial function. We found that S-9-PAHSA significantly enhanced spatial learning and memory abilities, reduced amyloid plaque deposition, decreased neuronal apoptosis, and improved mitochondrial homeostasis and autophagy in 5xFAD mice. These findings suggest that S-9-PAHSA holds promise as a supplementary preventive and therapeutic strategy for AD treatment.
    Keywords:  Alzheimer's disease; S‐9‐PAHSA; amyloid‐beta; cognition; mitochondrial autophagy
    DOI:  https://doi.org/10.1111/ejn.70118
  6. J Mol Biol. 2025 Apr 21. pii: S0022-2836(25)00227-X. [Epub ahead of print] 169161
    Mitophagy in Neurons: Mechanisms Regulating Mitochondrial Turnover and Neuronal Homeostasis.
    Bishal Basak, Erika L F Holzbaur.
      Mitochondrial quality control is instrumental in regulating neuronal health and survival. The receptor-mediated clearance of damaged mitochondria by autophagy, known as mitophagy, plays a key role in controlling mitochondrial homeostasis. Mutations in genes that regulate mitophagy are causative for familial forms of neurological disorders including Parkinson's disease (PD) and Amyotrophic lateral sclerosis(ALS). PINK1/Parkin-dependent mitophagy is the best studied mitophagy pathway, while more recent work has brought to light additional mitochondrial quality control mechanisms that operate either in parallel to or independent of PINK1/Parkin mitophagy. Here, we discuss our current understanding of mitophagy mechanisms operating in neurons to govern mitochondrial homeostasis. We also summarize progress in our understanding of the links between mitophagic dysfunction and neurodegeneration and highlight the potential for therapeutic interventions to maintain mitochondrial health and neuronal function.
    Keywords:  PINK1; Parkin; autophagosomes; lysosomes; mitochondria; mitophagy; neurodegeneration
    DOI:  https://doi.org/10.1016/j.jmb.2025.169161
  7. J Cachexia Sarcopenia Muscle. 2025 Apr;16(2): e13823
    ExermiR-129-3p Enhances Muscle Function by Improving Mitochondrial Activity Through PARP1 Inhibition.
    Yeo Jin Shin, Jae Won Yang, Heeyeon Jeong, Joyeong Kim, Bora Lee, Ji-Won Kim, Seung-Min Lee, Ju Yeon Kwak, Young Hoon Son, Kap Jung Kim, Yong Ryoul Yang, Chuna Kim, Ki-Sun Kwon, Kwang-Pyo Lee.
       BACKGROUND: Physical exercise has beneficial effects on various organs, including skeletal muscle. However, not all patients are capable of engaging in exercise to maintain muscle function, which underscores the importance of identifying molecular mechanisms of physical training that could lead to the discovery of exercise-mimicking molecules.
    METHODS: This study sought to identify molecular mediators of exercise that could improve muscle function. We focused on the exercise-induced microRNA (miR)-129-3p, investigating its role and effects on mitochondrial activity both in vivo and in vitro. The expression of miR-129-3p was analysed in skeletal muscle following exercise, and its downstream effects on the poly (ADP-ribose) polymerase-1 (Parp1)-SIRT1-PGC1α signalling pathway were elucidated. Functional studies were conducted using muscle-specific overexpression of miR-129-3p in adult mice and intramuscular injection of AAV9-miR-129-3p in obese mice to assess exercise capacity and muscle strength.
    RESULTS: Exercise was found to upregulate miR-129-3p in skeletal muscle (p < 0.05), which directly inhibits Parp1, a major NAD+-consuming enzyme. This inhibition leads to increased NAD+ levels (p < 0.05), activating SIRT1 and subsequently reducing the acetylation of PGC1α, thereby enhancing mitochondrial function. Muscle-specific overexpression of miR-129-3p in adult mice significantly enhanced exercise capacity (> 130%, p < 0.0001), while AAV9-miR-129-3p injections ameliorated muscle weakness (twitch force, > 140%, p < 0.05; tetanic force, > 160%, p < 0.01) in obese mice. In human skeletal muscle myoblasts, miR-129-3p improved mitochondrial function via the PARP1-SIRT1-PGC1α signalling pathway.
    CONCLUSION: Our findings suggest that miR-129-3p, induced by exercise, can mimic the beneficial effects of physical exercise. This highlights miR-129-3p as a potential therapeutic target for improving muscle health, especially in individuals unable to exercise.
    Keywords:  PARP1; TRIM63; exercise mimic; exermiR; microRNA; skeletal muscle
    DOI:  https://doi.org/10.1002/jcsm.13823
  8. Biochem Biophys Res Commun. 2025 Apr 16. pii: S0006-291X(25)00543-1. [Epub ahead of print]765 151829
    Mitochondrial calpain-1 truncates ATP synthase beta subunit.
    Yusaku Chukai, Nanami Furukawa, On Kosegawa, Lanlan Bai, Eriko Sugano, Tomokazu Fukuda, Hiroshi Tomita, Taku Ozaki.
      Calpains cleave proteins in a calcium concentration-dependent manner, modulating their intracellular functions. Calpain-1, a member of the calpain family, is localized in the cytosol and mitochondria. Mitochondrial calpain-1 induces mitochondrial dysfunction and apoptosis by cleaving its substrate. Thus, identifying the substrate of calpain-1 is essential to understand its function. However, little is known about the substrates of mitochondrial calpain-1. To address this issue, we screened mitochondrial proteins using bioinformatics approaches and two-dimensional gel electrophoresis. We identified ATP5B as a potential substrate of mitochondrial calpain-1. Calpeptin, a pan-calpain inhibitor, and Tat-μCL, a mitochondrial calpain-1 specific inhibitor, prevented the truncation of ATP5B during in vitro Ca2+ incubation. Using recombinant human calpain-1 and ATP5B proteins, we demonstrated that calpain-1 directly cleaved ATP5B, generating a fragment of ATP5B. Based on the predicted cleavage sites in ATP5B, this cleavage may disrupt its interaction with ATP5A1, leading to mitochondrial dysfunction in ATP production. This study identified ATP5B as a novel substrate of mitochondrial calpain-1. The results provide new insights into mitochondrial dysfunction.
    Keywords:  ATP5B; Calpain-1; Mitochondria
    DOI:  https://doi.org/10.1016/j.bbrc.2025.151829
  9. Sci Rep. 2025 Apr 22. 15(1): 13824
    The association between serum growth differentiation factor 15 and insulin resistance in women diagnosed with polycystic ovary syndrome.
    Yufeng Mei, Wanzhen Li, Zhenni Chen, Min Wang.
      Polycystic ovary syndrome (PCOS) is strongly associated with metabolic abnormalities, with 50-70% of patients exhibiting insulin resistance (IR), which significantly impacts the reproductive health of women in their reproductive years. Growth differentiation factor 15 (GDF15), a hormone responsive to nutritional stress, has been implicated in several diseases. This study sought to clarify the relationship between GDF15 levels and IR condition in PCOS patients. Based on the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), patients were categorized into an IR-PCOS group (n = 124) and a non-insulin-resistant group (non-IR-PCOS group, n = 109). Fasting blood samples were collected to measure GDF15 concentrations. To assess metabolic complications in relation to GDF15 levels, patients were also classified into high and normal GDF15 groups. Serum GDF15 levels were significantly higher in IR-PCOS patients (median 772.94 pg/ml) compared to non-IR-PCOS patients (median 575.80 pg/ml, P < 0.05). The high GDF15 group showed more severe metabolic and lipid abnormalities than the normal GDF15 group. Spearman correlation analysis revealed a correlation between increased GDF15 levels and impaired glucose metabolism. Logistic regression analysis identified GDF15, HDL-C, and prolactin as risk factors for IR in PCOS, and the fully adjusted regression coefficient for GDF15 levels and IR prevalence was 4.490 (95% CI 1.541 to 13.088). Restricted cubic spline analysis confirmed a positive association between GDF15 levels and IR within a specific range. The combined predictive probability of GDF15, prolactin, and HDL-C for IR was 0.763 (95% CI 0.701 to 0.826) according to ROC analysis. Elevated GDF15 levels may be associated with IR in PCOS patients, suggesting a potential role for GDF15 in the pathophysiology of IR in this condition.
    Keywords:  Growth differentiation factor 15; Insulin resistance; Polycystic ovarian syndrome
    DOI:  https://doi.org/10.1038/s41598-025-98028-6
  10. Nat Chem Biol. 2025 Apr 22.
    TOM20-driven E3 ligase recruitment regulates mitochondrial dynamics through PLD6.
    Anat Raiff, Shidong Zhao, Aizat Bekturova, Colin Zenge, Shir Mazor, Xinyan Chen, Wenwen Ru, Yaara Makaros, Tslil Ast, Alban Ordureau, Chao Xu, Itay Koren.
      Mitochondrial homeostasis is maintained through complex regulatory mechanisms, including the balance of mitochondrial dynamics involving fusion and fission processes. A central player in this regulation is the ubiquitin-proteasome system (UPS), which controls the degradation of pivotal mitochondrial proteins. In this study, we identified cullin-RING E3 ligase 2 (CRL2) and its substrate receptor, FEM1B, as critical regulators of mitochondrial dynamics. Through proteomic analysis, we demonstrate here that FEM1B controls the turnover of PLD6, a key regulator of mitochondrial dynamics. Using structural and biochemical approaches, we show that FEM1B physically interacts with PLD6 and that this interaction is facilitated by the direct association of FEM1B with the mitochondrial import receptor TOM20. Ablation of FEM1B or disruption of the FEM1B-TOM20 interaction impairs PLD6 degradation and induces mitochondrial defects, phenocopying PLD6 overexpression. These findings underscore the importance of FEM1B in maintaining mitochondrial morphology and provide further mechanistic insights into how the UPS regulates mitochondrial homeostasis.
    DOI:  https://doi.org/10.1038/s41589-025-01894-4
  11. Food Funct. 2025 Apr 22.
    Crocin extends lifespan by mitigating oxidative stress and regulating lipid metabolism through the DAF-16/FOXO pathway.
    Ai-Pei Li, Dan Li, Xin Tan, Rui Xu, Lin-Xi Mao, Juan-Juan Kang, Sheng-Hong Li, Yan Liu.
      Aging represents a significant global challenge characterized by persistent oxidative stress and dysregulated lipid metabolism. Crocin, the primary bioactive constituent of saffron (Crocus sativus L.), is widely utilized as a natural food colorant and exhibits potent anti-inflammatory and antioxidant properties. Previous studies have demonstrated crocin's antioxidative, neuroprotective and memory-enhancing effects in aged rats; however, its direct impact on aging and the underlying mechanisms remain unexplored. In this study, we demonstrated that crocin treatment extended lifespan, enhanced survival under heat and juglone-induced oxidative stress, and reduced lipofuscin accumulation in the model organism C. elegans. Mechanistically, crocin activated DAF-16, the C. elegans homolog of human FOXO, resulting in the upregulation of key antioxidant genes (gst-4, sod-3 and hsp-16.2). Notably, the lifespan-extension effect of crocin was abolished in a daf-16 mutant, and its antioxidant effects were significantly attenuated in daf-16 RNAi experiments conducted in N2, CL2166, CF1553 and TJ375 strains. Furthermore, crocin specifically reduced fat accumulation, and upregulated the expression of genes involved in lipid mobilization (lipl-3, lipl-4, atgl-1 and acs-2) and unsaturated fatty acid synthesis (fat-6 and elo-2) in aged nematodes. GC-MS analysis further demonstrated that crocin treatment elevated the levels of unsaturated fatty acids (C18:1n9, C20:4n-6, C20:4n-3 and C20:5n-3), an effect that was completely abolished under daf-16 knockdown conditions. Collectively, these findings suggest that crocin promotes longevity in C. elegans by mitigating oxidative stress and modulating lipid metabolism through the DAF-16/FOXO pathway. These results highlight the potential of crocin as a promising strategy for treating aging and age-related diseases.
    DOI:  https://doi.org/10.1039/d5fo01157d
  12. Sci Rep. 2025 Apr 21. 15(1): 13787
    The REDOX balance in the prefrontal cortex is positively modulated by aerobic exercise and altered by overfeeding.
    Deyvison Guilherme Martins Silva, Jonata Henrique de Santana, Elenilson Maximino Bernardo, Matheus Santos de Sousa Fernandes, Fatma Hilal Yagin, Fahaid Al-Hashem, Mariana P Fernandes, Jarlei Fiamoncini, Safaa M Elkholi, Claudia J Lagranha.
      While obesity rates increase worldwide, physical activity levels are reduced. Obesity and physical inactivity may be inversely related to the production of reactive oxygen species (ROS) and cause oxidative stress in the central nervous system. In this study, we aimed to investigate the effects of aerobic physical exercise on the oxidative balance of the prefrontal cortex of rats subjected to overnutrition during lactation. For this, male Wistar rats were subjected to overnutrition during lactation between postnatal day 3 to 21. On postnatal day 23, the two groups of animals were subdivided into trained and untrained animals. Trained rats were subjected to a treadmill training protocol for four weeks, five days/week, 60 min/day, at 50% of maximum running capacity. Our findings demonstrate that overnutrition impairs REDOX balance in the prefrontal cortex through increased prooxidants and reduced antioxidant defenses. On the contrary, exercise tends to restore most of these measures to control levels, possibly due to the increase in mRNA levels of Sirt1 and reduction in Il-6 in the prefrontal cortex. Overnutrition causes oxidative stress in the prefrontal cortex, while exercise re-covers most of its adverse effects through activating anti-inflammatory mechanisms.
    Keywords:  Brain; Exercise; Obesity; Oxidative stress
    DOI:  https://doi.org/10.1038/s41598-025-99303-2
  13. Front Psychiatry. 2025 ;16 1555144
    Restoration of mitochondrial energy metabolism by electroconvulsive therapy in adolescent and juvenile mice.
    Ning Du, Yu Xie, Dandan Geng, Jingran Li, Heyan Xu, Yuna Wang, Jijia Gou, Xiwen Tan, Xiaoming Xu, Lei Shi, Yujia Chen, Fengming Chen, Zixuan Zhou, Gang Liu, Li Kuang.
       Background: Adolescent depression is an increasingly serious public health issue, and traditional treatment methods often have side effects or limited efficacy. Electroconvulsive therapy (ECT), a widely used treatment for severe depression, has recently gained attention for its potential in treating adolescent depression. Previous studies suggest that mitochondrial dysfunction is closely related to the onset of depression. Therefore, investigating the mechanism by which ECT alleviates depressive symptoms through the improvement of mitochondrial energy metabolism is of great significance.
    Methods: This study employed the chronic unpredictable mild stress (CUMS) mouse model to assess the effects of ECT on depression-like behaviors through the sucrose preference test, open field test, and tail suspension test. Additionally, mitochondrial energy metabolism markers, including ATP levels, oxygen consumption rate (OCR), lactate, and pyruvate, were measured in both mouse and human plasma to evaluate the effects of ECT on mitochondrial function.
    Results: The results showed that ECT significantly improved depression-like and anxiety-like behaviors in mice, as evidenced by the reversal of abnormal behaviors in the sucrose preference test, open field test, and tail suspension test. Analysis of plasma mitochondrial energy metabolism markers revealed that ECT significantly increased ATP levels, restored OCR, reduced lactate accumulation, and increased pyruvate levels. These findings suggest that ECT alleviates depressive symptoms by restoring mitochondrial energy metabolism and improving brain energy supply.
    Conclusion: This study systematically explored the potential mechanism by which ECT alleviates adolescent depression through the improvement of mitochondrial energy metabolism. The results indicate that ECT not only effectively alleviates depressive symptoms but also provides new insights and experimental evidence for the treatment of adolescent depression through mitochondrial function restoration. Future research could further investigate how to combine drug treatments to enhance mitochondrial function, improve ECT efficacy, and evaluate the effects of ECT in different depression subtypes, providing guidance for personalized clinical treatment.
    Keywords:  adenosine triphosphate (ATP); adolescent depression; electroconvulsive therapy (ECT); lactic acid; mitochondrial energy metabolism
    DOI:  https://doi.org/10.3389/fpsyt.2025.1555144
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