Fasting as a precursor to high‐fat diet enhances mitochondrial resilience in Drosophila melanogaster DOI Creative Commons
Florence Hunter‐Manseau,

Simon B. Cormier,

Rebekah Strang

et al.

Insect Science, Journal Year: 2024, Volume and Issue: 31(6), P. 1770 - 1788

Published: March 21, 2024

Abstract Changes in diet type and nutrient availability can impose significant environmental stress on organisms, potentially compromising physiological functions reproductive success. In nature, dramatic fluctuations dietary resources are often observed adjustments to restore cellular homeostasis crucial survive this of stress. study, we exposed male Drosophila melanogaster two modulated treatments: one without a fasting period before exposure high‐fat the other with 24‐h period. We then investigated mitochondrial metabolism molecular responses these treatments. Exposure preceding resulted disrupted respiration, notably at level complex I. On hand, short maintained respiration. Generally, transcript abundance genes associated mitophagy, heat‐shock proteins, biogenesis, sensing pathways increased either slightly or significantly following remained stable when flies were subsequently put diet, whereas drastic decrease almost all abundances was for directly diet. Moreover, enzymatic activities showed less variation after than treatment Overall, our study sheds light mechanistic protective effects prior highlights metabolic flexibility mitochondria response abrupt changes have implication adaptation species their changing environment.

Language: Английский

Mitochondria at the crossroads of health and disease DOI Creative Commons
Anu Suomalainen, Jodi Nunnari

Cell, Journal Year: 2024, Volume and Issue: 187(11), P. 2601 - 2627

Published: May 1, 2024

Mitochondria reside at the crossroads of catabolic and anabolic metabolism—the essence life. How their structure function are dynamically tuned in response to tissue-specific needs for energy, growth repair, renewal is being increasingly understood. respond intrinsic extrinsic stresses can alter cell organismal by inducing metabolic signaling within cells distal tissues. Here, we review how centrality mitochondrial functions manifests health a broad spectrum diseases aging.

Language: Английский

Citations

105
Envisioning how to advance the MASH field DOI
Alina M. Allen, Zobair M. Younossi, Anna Mae Diehl

et al.

Nature Reviews Gastroenterology & Hepatology, Journal Year: 2024, Volume and Issue: unknown

Published: June 4, 2024

Language: Английский

Citations

13
PRKN-linked familial Parkinson’s disease: cellular and molecular mechanisms of disease-linked variants DOI Creative Commons
Lene Clausen, Justyna Okarmus, Vasileios Voutsinos

et al.

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: May 20, 2024

Abstract Parkinson’s disease (PD) is a common and incurable neurodegenerative disorder that arises from the loss of dopaminergic neurons in substantia nigra mainly characterized by progressive motor function. Monogenic familial PD associated with highly penetrant variants specific genes, notably PRKN gene, where homozygous or compound heterozygous loss-of-function predominate. encodes Parkin, an E3 ubiquitin-protein ligase important for protein ubiquitination mitophagy damaged mitochondria. Accordingly, Parkin plays central role mitochondrial quality control but itself also subject to strict system rapidly eliminates certain disease-linked variants. Here, we summarize cellular molecular functions highlighting various mechanisms which gene result loss-of-function. We emphasize importance high-throughput assays computational tools clinical classification how detailed insights into pathogenic may impact development personalized therapeutics.

Language: Английский

Citations

9
The brain–body energy conservation model of aging DOI
Evan D. Shaulson, Alan A. Cohen, Martin Picard

et al.

Nature Aging, Journal Year: 2024, Volume and Issue: 4(10), P. 1354 - 1371

Published: Oct. 8, 2024

Language: Английский

Citations

7
Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress DOI Creative Commons
Sean M. Gettings,

William Timbury,

Anna Dmochowska

et al.

NanoImpact, Journal Year: 2024, Volume and Issue: 34, P. 100508 - 100508

Published: April 1, 2024

The objective of this investigation was to evaluate the influence micro- and nanoplastic particles composed polyethylene terephthalate (PET), a significant contributor plastic pollution, on human brain vascular pericytes. Specifically, we delved into their impact mitochondrial functionality, oxidative stress, expression genes associated with ferroptosis functions. Our findings demonstrate that exposure monoculture pericytes PET in vitro at concentration 50 μg/ml for duration 3, 6 10 days did not elicit stress. Notably, observed reduction various aspects respiration, including maximal spare respiratory capacity, ATP production subjected 3 days, function recovery days. Furthermore, there were no statistically alterations DNA copy number, or linked stress ferroptosis, but an increase gene transcription factor A (TFAM) noted exposure. These outcomes suggest that, μg/ml, do induce Instead, exposure, impairs functions, is recovered 6-day This seems indicate potential hormesis response (mitohormesis) incited, involving TFAM. Further investigations are warranted explore stages mitohormesis consequences plastics integrity blood-brain barrier intercellular interactions. research contributes our comprehension repercussions pollution health underscores imperative need ongoing examinations particles.

Language: Английский

Citations

6
Remote ischemic preconditioning prevents high‐altitude cerebral edema by enhancing glucose metabolic reprogramming DOI Creative Commons
Rongrong Han,

Xiaoyan Yang,

Xunming Ji

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(9)

Published: Sept. 1, 2024

Abstract Aims Incidence of acute mountain sickness (AMS) ranges from 40%–90%, with high‐altitude cerebral edema (HACE) representing a life‐threatening end stage severe AMS. However, practical and convenient preventive strategies for HACE are lacking. Remote ischemic preconditioning (RIPC) has demonstrated effects on ischemia‐ or hypoxia‐induced cardiovascular cerebrovascular diseases. This study aimed to investigate the potential molecular mechanism application RIPC in preventing onset. Methods A hypobaric hypoxia chamber was used simulate environment 7000 meters. Metabolomics metabolic flux analysis were employed assay metabolite levels. Transcriptomics quantitative real‐time PCR (q‐PCR) gene expression Immunofluorescence staining performed neurons label cellular proteins. The fluorescent probes Mito‐Dendra2, iATPSnFR1.0, CMTMRos observe mitochondria, ATP, membrane cultured neurons, respectively. TUNEL detect quantify apoptotic cell death. Hematoxylin eosin (H&E) utilized analyze pathological changes, such as tissue swelling cortex samples. Rotarod test assess motor coordination balance rats. Oxygen–glucose deprivation (OGD) cells an vitro model hypoglycemia induced by animal experiments. Results We revealed causative perturbation glucose metabolism brain preceding edema. Ischemic treatment significantly reprograms metabolism, ameliorating apoptosis energy deprivation. Notably, improves mitochondrial ATP production through enhanced glucose‐coupled metabolism. In vivo studies confirm that alleviates edema, reduces hypoxia, dysfunction resulting Conclusions Our elucidates basis pathogenesis. provides new strategy reprogramming highlighting targeting neuroprotective interventions neurological diseases caused ischemia hypoxia.

Language: Английский

Citations

5
Neurodegenerative disorders, metabolic icebergs, and mitohormesis DOI Creative Commons
Matthew Phillips, Martin Picard

Translational Neurodegeneration, Journal Year: 2024, Volume and Issue: 13(1)

Published: Sept. 6, 2024

Language: Английский

Citations

4
Altered mitochondrial unfolded protein response and FGF21 secretion in MASLD progression and the effect of exercise intervention DOI Creative Commons
Xinmeng Yuan, Wen Sun,

Ye Xu

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 29, 2025

Language: Английский

Citations

0
Transgenerational Inheritance of Mitochondrial Hormetic Oxidative Stress Mediated by Histone H3K4me3 and H3K27me3 Modifications DOI Creative Commons

Yimin Li,

Chongyang Wang,

Xiaoxia Fu

et al.

Redox Biology, Journal Year: 2025, Volume and Issue: 82, P. 103598 - 103598

Published: March 15, 2025

Mitochondrial hormetic oxidative stress (mtHOS) is crucial in physiology and disease; however, its effects on epigenetic inheritance organism fitness across generations remains elusive. Utilizing the C. elegans as a model, we elucidate that parental exposure to mtHOS not only elicits lifespan extension exposed individuals but also confers this longevity advantage progeny through transgenerational (TEI) mechanism. This transmission of prolongation depends activation UPRmt synergistic action transcription factors DAF-16/FOXO SKN-1/Nrf2. Additionally, H3K4me3 H3K27me3 serve mediators, selectively marking regulating expression genes associated with response determination. Our findings illuminate mechanisms underlying implementation mtHOS, revealing sophisticated interplay among chromatin remodeling collectively enhances progeny's adaptive resilience future challenges.

Language: Английский

Citations

0
Cellular stress and macrophage activation DOI
Jing Yu, Bin‐Zhi Qian

Seminars in Immunology, Journal Year: 2025, Volume and Issue: 78, P. 101953 - 101953

Published: April 12, 2025

Language: Английский

Citations

0