bims-mitmed 2025-10-26 papers

bims-mitmed

Biomed News

on Mitochondrial medicine

Issue of 2025–10–26
thirteen papers selected by
Dario Brunetti, Fondazione IRCCS Istituto Neurologico

Macular OCT inner retinal changes reflect CNS involvement in m.3243A>G disease.
Nanomaterial-induced mitochondrial biogenesis enhances intercellular mitochondrial transfer efficiency.
Stem-cell-derived extracellular vesicles in neurodegeneration and neuroaging: therapeutic potential and challenges.
Clinical utility of the ATP hydrolysis assay for the diagnosis of complex V deficiency in cultured skin fibroblasts.
Positron emission tomography reveals increased myocardial glucose uptake in a subset of Friedreich ataxia patients.
Development of an AAV-Based Gene Therapy for the Ocular Phenotype of Friedreich's Ataxia.
ZC3H4, a novel regulator of mitochondrial complex I, impacts prostate stromal cell senescence, attachment, adhesion and anoikis resistance.
Disrupting mitochondrial β-oxidation by depletion of HADHA impairs primary ciliogenesis.
Oligodendrocyte precursor cell-specific blocking of low-glucose-induced activation of AMPK ensures myelination and remyelination.
The multifaceted role of autophagy and mitophagy in cardiovascular health and disease.
Mitochondrial one-carbon metabolism is required for TGF-β-induced glycine synthesis and fibrotic responses.
Mitochondrial dysfunction in age-related sarcopenia: mechanistic insights, diagnostic advances, and therapeutic prospects.
Mitochondrial fatty acid oxidation is stimulated by red light irradiation.

BMJ Neurol Open. 2025 ;7(2): e001232

Macular OCT inner retinal changes reflect CNS involvement in m.3243A>G disease.

Hatem Jouda, Andrew C Browning, Akhunzada M Aftab, Ikhlas Mahmoud, Saima Bibi, Robert McFarland, Sarah J Pickett, Helen Devine.

   Background: The m.3243A>G mitochondrial DNA variant is the most common cause of adult mitochondrial disease and is associated with a heterogeneous clinical phenotype. The retina and optic nerve are among the most metabolically active tissues, making them vulnerable to mitochondrial dysfunction. Optical coherence tomography (OCT) studies have demonstrated retinal nerve fibre layer (RNFL) thinning in mitochondrial and other neurodegenerative diseases. We investigated whether temporal RNFL thinning is associated with central nervous system (CNS) involvement in individuals with the m.3243A>G variant.
Methods: High-resolution OCT was used to assess peripapillary RNFL thickness and perform macular segmentation. Participants were categorised into normal RNFL (n=14) or temporal RNFL thinning (n=15) groups. Demographic data, mean-corrected m.3243A>G heteroplasmy, Newcastle Mitochondrial Disease Adult Scale (NMDAS) scaled scores and NMDAS neurological traits were compared.
Results: Temporal RNFL thinning was significantly associated with neurological features (Fisher's exact test, p=0.027). In multivariable analysis, RNFL thinning and age were independent predictors of neurological involvement. Macular OCT revealed concomitant thinning of the ganglion cell-inner plexiform (GC-IPL) complex in the RNFL thinning group, with preservation of outer retinal layers, supporting primary retinal ganglion cell vulnerability. No significant associations were found between RNFL thinning and m.3243A>G heteroplasmy or NMDAS scaled scores.
Conclusion: Temporal RNFL thinning, accompanied by GC-IPL loss, is associated with neurological involvement in m.3243A>G-related mitochondrial disease, supporting its potential as a non-invasive biomarker of CNS dysfunction. Longitudinal studies are needed to determine whether these retinal changes are progressive and predictive of neurological decline.

Keywords:  CLINICAL NEUROLOGY; MITOCHONDRIAL DISORDERS; NEUROMUSCULAR; NEUROOPHTHALMOLOGY

DOI:  https://doi.org/10.1136/bmjno-2025-001232
Proc Natl Acad Sci U S A. 2025 Oct 28. 122(43): e2505237122

Nanomaterial-induced mitochondrial biogenesis enhances intercellular mitochondrial transfer efficiency.

John Soukar, Kanwar Abhay Singh, Ari Aviles, Sarah Hargett, Harman Kaur, Samantha Foster, Shounak Roy, Feng Zhao, Vishal M Gohil, Irtisha Singh, Akhilesh K Gaharwar.

  Intercellular mitochondrial transfer, the spontaneous exchange of mitochondria between cells, is a recently described phenomenon crucial for cellular repair, regeneration, and disease management. Enhancing this natural process holds promise for developing novel therapies targeting diseases associated with mitochondrial dysfunction. Here, we introduce a nanomaterial-based approach employing molybdenum disulfide (MoS2) nanoflowers with atomic-scale vacancies to stimulate mitochondrial biogenesis in cells to make them mitochondrial biofactories. Upon cellular uptake, these nanoflowers result in a two-fold increase in mitochondrial mass and enhancing mitochondrial transfer to recipient cells by several-fold. This enhanced efficiency of transfer significantly improves mitochondrial respiratory capacity and adenosine triphosphate production in recipient cells under physiological conditions. In cellular models of mitochondrial and cellular damage, MoS2 enhanced mitochondrial transfer achieved remarkable restoration of cell function. This proof-of-concept study demonstrates that nanomaterial-boosted intercellular mitochondrial transfer can enhance cell survivability and function under diseased conditions, offering a promising strategy for treating mitochondrial dysfunction-related diseases.

Keywords:  biomaterials; cellular medicine; mitochondria; nanomaterials; regenerative medicine

DOI:  https://doi.org/10.1073/pnas.2505237122
Extracell Vesicles Circ Nucl Acids. 2025 ;6(3): 594-608

Stem-cell-derived extracellular vesicles in neurodegeneration and neuroaging: therapeutic potential and challenges.

Mohit Kumar, Sudipta Ray, Susmita Sil.

  Neuroaging is a complex biological process in which the brain undergoes progressive functional decline marked by synaptic loss, neuroinflammation, and cognitive decline. At the molecular and cellular level, aging is driven by multiple interconnected hallmarks, including genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. Among these, cellular senescence, a state of irreversible cell cycle arrest, has emerged as a critical contributor to brain aging. Senescent cells accumulate with age, driven by the p53-p21 and p16-pRb pathways, and secrete pro-inflammatory factors via senescence-associated secretory phenotype (SASP), thereby exacerbating neurodegeneration, vascular dysfunction, and cognitive decline. Extracellular vesicles (EVs) are natural nanocarriers of proteins, lipids, and nucleic acids, and have emerged as key mediators of intercellular communication and therapeutics for aging and age-related conditions. EVs derived from various cell types, such as mesenchymal stem cells (MSCs), neural stem cells (NSCs), and induced pluripotent stem cells (iPSCs), can modulate senescence-related pathways, reduce inflammation, and promote tissue repair. Preclinical studies demonstrate that stem-cell-derived EVs can improve cognitive performance, enhance neurogenesis, reduce senescence phenotype, improve neuronal survival through neuroprotective miRNAs (miR-181a-2-3p), suppress neuroinflammation via inhibition of NLRP3 inflammasome, and support synaptic plasticity. Stem cell EVs possess natural biocompatibility, the ability to cross the blood-brain barrier (BBB), and targeted delivery mechanisms, making them promising candidates for anti-aging interventions. This review elaborates on the multifaceted role of stem cell EVs in mitigating brain aging, senescence, and age-associated chronic disease phenotype.

Keywords:  Brain aging; extracellular vesicles; neurodegeneration; stem cell therapy

DOI:  https://doi.org/10.20517/evcna.2025.65
Mol Genet Metab. 2025 Oct 06. pii: S1096-7192(25)00249-5. [Epub ahead of print]146(3): 109257

Clinical utility of the ATP hydrolysis assay for the diagnosis of complex V deficiency in cultured skin fibroblasts.

Marisa W Friederich, Johan L K Van Hove.

  Complex V catalyzes the formation of ATP from ADP and Pi through the dissipation of the proton gradient generated during the process of oxidative phosphorylation. Most complex V genetic disorders are caused by missense mutations in the mtDNA-encoded subunits, a (MT-ATP6) and A6L (MT-ATP8). Nuclear DNA-encoded gene mutations are increasingly recognized as causes of complex V defects and exhibited both autosomal recessive and autosomal dominant inheritance. Most identified variants are novel and confirmation by functional assays is important especially for variants demonstrating autosomal dominant inheritance. A kinetic spectrophotometric assay of the Complex V enzymatic hydrolysis activity has been reported. Here we report the clinical utility of this assay for the diagnosis of complex V deficiency after optimization and validation for the diagnosis of isolated complex V disorders due to both nuclear and mitochondrial DNA encoded variants and also for use in combined respiratory chain deficiencies. This assay was able to identify all nuclear DNA-encoded complex V deficiencies, whereas a decrease in complex V activity was observed in some patient cell lines with combined deficiencies. However, this assay only identified 50% of the mitochondrial DNA-encoded complex V deficiencies due to pathogenic variants in MT-ATP6/8. In conclusion, the enzymatic assay of complex V has best clinical utility for nuclear DNA-encoded complex V defects.

Keywords:  ATP synthase; Clinical utility; Complex V; Enzyme assay; Sensitivity

DOI:  https://doi.org/10.1016/j.ymgme.2025.109257
Sci Rep. 2025 Oct 24. 15(1): 37247

Positron emission tomography reveals increased myocardial glucose uptake in a subset of Friedreich ataxia patients.

R Mark Payne, Thomas M O'Connell, P Melanie Pride, Gregg R Wagner, George J Eckert, Tiffany R Johnson, Weinian Shou, Gary D Hutchins.

Why some but not all patients with the rare disease Friedreich ataxia (FRDA) are at increased risk of poor cardiovascular outcome and death is unclear and unpredictable. We investigated the hypothesis that mitochondrial dysfunction in FRDA leads to altered patterns of myocardial metabolic substrate utilization. We recruited 5 healthy controls (Ctl) and 11 FRDA participants. All underwent fasting myocardial positron emission tomography (PET scan) with 15O-H2O, 18F-FDG, and 11C-Palmitate. We conducted cardiac transcriptomics on mice with ablation of the Frda gene in heart to explore mechanisms of fuel substrate utilization. Five (45%) FRDA participants had an LV mass index (LVMi) less than 51 g/m2.7 (Group I), and 6 (55%) FRDA participants had an LVMi greater than this (Group II). 73% (8/11) of all FRDA participants had evidence of increased myocardial FDG uptake relative to controls. All of Group II had FDG/Palmitate utilization ratios > 95% versus controls, as well as cTnI leak (p = 0.007) when compared to Ctl (p = 0.008) or Group I (p = 0.022). RNA transcriptomics from FRDA mouse heart showed upregulation of genes for glucose uptake and glycolysis with decreased genes associated with mitochondrial energy production. In summary, PET scan identified 2 metabolically distinct subclasses of FRDA cardiomyopathy. FRDA participants with an LVMi greater than 51 g/m2.7 had greater FDG uptake than those with an LVMi less than 51 g/m2.7, or Ctl, and this correlated with LV systolic and diastolic dysfunction. Supporting this finding, gene expression in the FRDA mouse heart shifts to favor glycolysis with decreased mitochondrial energy production.

DOI: https://doi.org/10.1038/s41598-025-21330-w
Mol Ther. 2025 Oct 23. pii: S1525-0016(25)00869-X. [Epub ahead of print]

Development of an AAV-Based Gene Therapy for the Ocular Phenotype of Friedreich's Ataxia.

Heyu Tang, Siddhant Gupte, Emily Xu, Kaitlyn R Calabro, Hannah Friend, Sean M Crosson, Diego Fajardo, Zachary Kostamo, Hangning Zhang, James J Peterson, Fangyu Lin, Zbynek Kozmik, Cathleen M Lutz, Sanford L Boye, Shannon E Boye.

Friedreich's Ataxia (FA) is a leading form of hereditary ataxia caused by autosomal recessive mutations in frataxin (FXN). GAA triplet repeat expansions lead to lower levels of FXN expression, abnormal influx of iron into mitochondria and damage to the nervous system. Patients typically present before the second decade with loss of muscular function, speech impediments, and cardiomyopathy. At later stages, vision loss typically manifests. Work is underway to develop gene therapies that address the cardiac and CNS manifestations, but their routes of administration do not lead to efficient transduction of the retina. The purpose of this study was to develop a more direct approach for treating the ocular phenotype of FA which includes loss of retinal ganglion cells (RGCs), thinning of the retinal nerve fiber layer (RNFL), optic nerve atrophy, and loss of visual field. We generated two novel conditional knock-out (KO) models, mRx-Fxn KO and Pou4f2-Fxn KO mice, wherein Fxn is ablated in all retinal cells or RGCs, respectively and showed that FXN deficiency led to retinal dystrophy in both models. Gene supplementation via intravitreal injection of a novel AAV2-based capsid carrying FXN partially preserved retinal structure and/or function in both models, establishing proof-of-concept for this therapeutic strategy.

DOI: https://doi.org/10.1016/j.ymthe.2025.10.048
Cell Death Dis. 2025 Oct 21. 16(1): 741

ZC3H4, a novel regulator of mitochondrial complex I, impacts prostate stromal cell senescence, attachment, adhesion and anoikis resistance.

Teresa T Liu, Mia J Carrarini, Livianna K Myklebust, Kegan O Skalitzky, Nathalie El-Khoury, Ian J Sipula, Alexander Chang, Vishal Soman, Ailing Liu, Nnamdi Ihejirika, Uma R Chandran, Michael J Jurczak, William A Ricke, Donald B DeFranco, Laura E Pascal.

Declining mitochondrial function is an established feature of aging and contributes to most aging-related diseases through its impact on various pathologies such as chronic inflammation, fibrosis and cellular senescence. Our recent work suggests that benign prostatic hyperplasia, which is an aging-related disease frequently associated with inflammation, fibrosis and senescence, is characterized by a decline in mitochondrial function. Here, we utilize glycolytic restriction and pharmacologic inhibition of the mitochondrial electron transfer chain complex I to promote mitochondrial dysfunction and identify the cellular processes impacted by declining mitochondrial function in benign prostate stromal cells. Using this model, we show that mitochondrial dysfunction induced alterations in cell-cell and cell-matrix adhesion, elevated fibronectin expression, resistance to anoikis and stress-induced premature senescence (SIPS). We also showed that ablation of ZC3H4, a transcription termination factor implicated in anoikis-resistance and reduced in BPH relative to normal prostates, phenocopied various phenotypes in the human BHPrS1 prostate stromal cell line that resulted from inhibition of complex I. Furthermore, ZC3H4 ablation resulted in the elevation of mitochondrial superoxide (mtROS) and mitochondrial membrane potential, altered mitochondrial morphology and NAD+/NADH ratio, and reduced CI function in BHPrS1 cells. Thus, ZC3H4 loss promotes mitochondrial dysfunction to drive pathophysiologic changes in the stromal compartment that are features of the aging prostate.

DOI: https://doi.org/10.1038/s41419-025-08027-8
Sci Rep. 2025 Oct 21. 15(1): 36544

Disrupting mitochondrial β-oxidation by depletion of HADHA impairs primary ciliogenesis.

Joon Bum Kim, Yong Hwan Kim, Seong Hyun Kim, Hyejin Hyung, Jun Hee So, Daeun Park, Na Yeon Park, Dong Kyu Choi, Ji-Eun Bae, Dong-Hyung Cho.

  Primary cilia are dynamic signaling hubs essential for cell homeostasis, and defects in ciliogenesis underpin various genetic disorders. Alpha-hydroxyacyl-CoA dehydrogenase (HADHA), a subunit of the mitochondrial trifunctional enzyme, is crucial for long-chain fatty acid β-oxidation and acetyl-CoA production. Although it was recently demonstrated that lipid metabolism modulates primary ciliogenesis, the connection between mitochondrial β-oxidation and primary cilia remains largely unexplored. Here, we report that HADHA dysfunction markedly impairs primary ciliogenesis and disrupts cilia-dependent signaling. Loss of HADHA reduces both ciliary frequency and length, accompanied by decreased levels of key ciliary signaling mediators. Reintroduction of wild-type HADHA in HADHA knockout cells rescues these defects, whereas its dehydrogenase deficiency mutant (E510Q) fails to restore either normal cilia formation or ciliary signaling. Notably, supplementation with sodium acetate, which resupplies intracellular acetyl-CoA, effectively rescues primary cilium in HADHA-deficient cells. Importantly, this acetate-mediated rescue implicates a potential therapeutic strategy for HADHA-related disorders, supporting the translational relevance of modulating acetyl-CoA levels to restore ciliary function. These findings suggest a relevant link between mitochondrial β-oxidation and primary ciliogenesis, highlighting acetyl-CoA as a potential therapeutic target for disorders related to HADHA deficiency.

Keywords:  Acetyl-CoA; Ciliopathy; HADHA; Primary cilia; β-oxidation

DOI:  https://doi.org/10.1038/s41598-025-18451-7
Nat Metab. 2025 Oct 22.

Oligodendrocyte precursor cell-specific blocking of low-glucose-induced activation of AMPK ensures myelination and remyelination.

Yuxia Sun, Wei-Wei Zhang, Lu Men, Jianfeng Wu, Luming Yao, Xi Huang, Yaying Wu, Cixiong Zhang, Ying Chen, David Carling, Chen-Song Zhang, Sheng-Cai Lin.

It has been shown that in most cells, low glucose leads to activation of AMP-activated protein kinase (AMPK) via the lysosomal glucose-sensing pathway, where glycolytic aldolase acts as the glucose sensor. Here, we show that ALDOC (aldolase C), the predominant isozyme of aldolase in mouse and rat oligodendrocyte precursor cells (OPCs), is acetylated at lysine 14, making the lysosomal glucose-sensing AMPK pathway unable to operate. We find that the blockage of AMPK activation is required for the proper proliferation and differentiation of OPCs into mature oligodendrocytes for myelination during development and for remyelination in areas of demyelination where the local glucose levels are low. Therefore, the acetylation of aldolase acts as a checkpoint for AMPK activation in response to low glucose to ensure the proliferation and differentiation of OPCs for myelination, and remyelination of demyelinated neurons.

DOI: https://doi.org/10.1038/s42255-025-01386-8
Autophagy Rep. 2025 ;4(1): 2572511

The multifaceted role of autophagy and mitophagy in cardiovascular health and disease.

Mireia Nàger, Mauro Calvoli, Kenneth B Larsen, Asa B Birgisdottir.

  The cardiovascular system, consisting of the heart and blood vessels, ensures delivery of oxygen and nutrient-rich blood throughout the whole body. The major cell types include cardiomyocytes, endothelial cells, and vascular smooth muscle cells. Dramatic consequences, sometimes with a deadly outcome, may arise when the activity of cardiovascular cells is compromised. The cardiomyocytes are terminally differentiated cells and thus do not normally regenerate. To sustain the high energy demand of the beating heart, the cardiomyocytes contain a high amount of energy producing mitochondria. Adaptation to metabolic demands is an integral part of cellular homeostasis and involves autophagy. Autophagy is an evolutionary conserved intracellular degradation pathway of cellular constituents. Mitophagy refers to selective degradation of damaged, and thus potentially harmful, mitochondria through autophagy. Both autophagy and mitophagy are widely implicated in physiological and pathological processes within cardiovascular cells. In this review, we highlight studies applying genetic modifications in mouse models to reveal the impact of autophagy and mitophagy on cardiovascular health and disease.

Keywords:  Aging; atherosclerosis; development; genetic mouse models; heart failure; myocardial infarction

DOI:  https://doi.org/10.1080/27694127.2025.2572511
Nat Commun. 2025 Oct 20. 16(1): 9250

Mitochondrial one-carbon metabolism is required for TGF-β-induced glycine synthesis and fibrotic responses.

Angelo Y Meliton, Kun Woo D Shin, Rengül Cetin-Atalay, M Volkan Atalay, Yufeng Tian, Jennifer C Houpy Szafran, Takugo Cho, Kaitlyn A Sun, Parker S Woods, Obada R Shamaa, Bohao Chen, Nickolai O Dulin, Aliya N Husain, Alexander Muir, Hardik Shah, Gökhan M Mutlu, Robert B Hamanaka.

TGF-β-dependent activation of lung fibroblasts is a hallmark of Idiopathic Pulmonary Fibrosis (IPF) which results in excessive collagen deposition and progressive scarring. Collagen production by lung fibroblasts is supported by de novo synthesis of glycine, the most abundant amino acid in collagen protein. SHMT2 produces glycine by transferring a one-carbon (1 C) unit from serine to tetrahydrofolate (THF), producing 5,10-methylene-THF (meTHF). meTHF is then converted back to THF in the mitochondrial 1 C pathway. It is unknown how 1 C metabolism contributes to collagen protein production and fibrosis. Here, we demonstrate that TGF-β induces the expression of mitochondrial 1 C pathway enzymes, including MTHFD2, in human lung fibroblasts. MTHFD2 was required for TGF-β-induced cellular glycine accumulation and collagen protein production in lung fibroblasts. Pharmacologic inhibition of MTHFD2 ameliorated fibrotic responses after intratracheal bleomycin instillation in vivo. Our findings suggest that mitochondrial 1 C metabolism is a therapeutic target for IPF and other fibrotic diseases.

DOI: https://doi.org/10.1038/s41467-025-64320-2
Front Cell Dev Biol. 2025 ;13 1590524

Mitochondrial dysfunction in age-related sarcopenia: mechanistic insights, diagnostic advances, and therapeutic prospects.

Yingtao Huang, Chenchen Wang, Haijian Cui, Guangjiang Sun, Xiaonan Qi, Xiaosheng Yao.

  Sarcopenia is a progressive age-related decline in skeletal muscle mass, strength, and function, representing a significant health burden in older adults. Diagnostic criteria have been established that integrate measures of muscle mass, strength, and physical performance [e.g., European Working Group on Sarcopenia in Older People 2010 (EWGSOP1) and 2019 (EWGSOP2) criteria]. Mechanistically, sarcopenia is driven by hormonal changes, chronic inflammation, cellular senescence, and, importantly, mitochondrial dysfunction. Age-related declines in sex hormones and activation of myostatin impair muscle regeneration and metabolism, while chronic low-grade inflammation disrupts protein synthesis and accelerates proteolysis via the ubiquitin-proteasome system (UPS) and autophagy-lysosome pathway (ALP). The accumulation of senescent cells and their secretory phenotype further exacerbates muscle degeneration and functional decline. Mitochondrial dysfunction plays a central role, characterized by impaired biogenesis, excessive reactive oxygen species (ROS) production, compromised autophagy/mitophagy, and accumulation of mitochondrial DNA (mtDNA) mutations. These defects collectively disrupt muscle energy homeostasis, promoting atrophy. The AMPK/SIRT1/PGC-1α and mTORC1 signaling pathways, along with PINK1/Parkin-mediated and receptor-dependent mitophagy, are essential for regulating mitochondrial biogenesis, protein synthesis, and mitochondrial quality control. Current and emerging therapeutic approaches include resistance and endurance exercise, nutritional and pharmacological agents targeting mitochondrial health, and hormonal modulation. Innovative treatments such as senolytics, exerkines, and gene therapies show promise but require further validation. Future advances in mechanistic understanding, diagnostics, and therapeutic strategies offer hope for mitigating sarcopenia and improving the quality of life in aging populations.

Keywords:  aging; chronic inflammation; mitochondrial dysfunction; muscle atrophy; sarcopenia; therapeutic strategies

DOI:  https://doi.org/10.3389/fcell.2025.1590524
FEBS Lett. 2025 Oct 18.

Mitochondrial fatty acid oxidation is stimulated by red light irradiation.

Manuel Alejandro Herrera, Camille C Caldeira da Silva, Maiza Von Denz, Mauricio S Baptista, Alicia J Kowaltowski.

  Keratinocytes are the primary constituents of sunlight-exposed epidermis. In these cells, ultraviolet (UV) A light completely inhibited oxidative phosphorylation, while equivalent doses of blue and green light preserved metabolic fluxes but reduced viability. In contrast, red light enhanced proliferation and elevated basal and maximal oxygen consumption rates for 48 h without altering protein levels of the electron transport chain. Targeted flux analysis revealed that red light specifically activates AMP-activating protein kinase (AMPK)-dependent mitochondrial fatty acid oxidation. This was accompanied by reduced levels of free fatty acids and increased acetyl-CoA carboxylase phosphorylation. Together, our results characterize wavelength-selective regulation of keratinocyte metabolism: UV/visible wavelengths induce damage, while red light triggers AMPK-dependent fatty acid oxidation, providing a mechanistic explanation for photobiomodulation in epidermal cells. Impact statement Sunlight impacts skin cells in surprising ways. While UVA harms energy production and blue/green light reduces survival, red light boosts keratinocyte metabolism. We show that red light activates AMPK-dependent fatty acid oxidation, enhancing proliferation and energy use. These findings reveal how specific wavelengths can damage or stimulate skin cells.

Keywords:  AMPK; beta oxidation; light; metabolism; mitochondria; skin

DOI:  https://doi.org/10.1002/1873-3468.70195