Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship DOI
Yousong Zhu,

Qinlong Hui,

Zheng Zhang

et al.

Journal of Neuroscience Research, Journal Year: 2024, Volume and Issue: 102(2)

Published: Feb. 1, 2024

Abstract Synapses serve as the points of communication between neurons, consisting primarily three components: presynaptic membrane, synaptic cleft, and postsynaptic membrane. They transmit signals through release reception neurotransmitters. Synaptic plasticity, ability synapses to undergo structural functional changes, is influenced by proteins such growth‐associated proteins, vesicle density neurotrophic growth factors. Furthermore, maintaining plasticity consumes more than half brain's energy, with a significant portion this energy originating from ATP generated mitochondrial metabolism. Consequently, quantity, distribution, transport, function mitochondria impact stability brain metabolism, thereby participating in regulation fundamental processes including neuronal differentiation, neurite outgrowth, synapse formation, neurotransmitter release. This article provides comprehensive overview associated common factors two, well relationship metabolism plasticity.

Language: Английский

Exposure to 6-PPD quinone causes damage on mitochondrial complex I/II associated with lifespan reduction in Caenorhabditis elegans DOI

Xin Hua,

Geyu Liang, Jie Chao

et al.

Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 472, P. 134598 - 134598

Published: May 13, 2024

Language: Английский

Citations

20

Mitochondrial dysfunction and therapeutic perspectives in osteoporosis DOI Creative Commons
Jialing Liu,

Zhonghua Gao,

Xiangjie Liu

et al.

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 2, 2024

Osteoporosis (OP) is a systemic skeletal disorder characterized by reduced bone mass and structural deterioration of tissue, resulting in heightened vulnerability to fractures due increased fragility. This condition primarily arises from an imbalance between the processes resorption formation. Mitochondrial dysfunction has been reported potentially constitute one most crucial mechanisms influencing pathogenesis osteoporosis. In essence, mitochondria play role maintaining delicate equilibrium formation resorption, thereby ensuring optimal health. Nevertheless, disruption this balance can arise as consequence mitochondrial dysfunction. dysfunctional mitochondria, electron transport chain (ETC) becomes uncoupled, ATP synthesis generation reactive oxygen species (ROS). Reinforcement further exacerbated accumulation aberrant mitochondria. review, we investigated analyzed correlation dysfunction, encompassing DNA (mtDNA) alterations, oxidative phosphorylation (OXPHOS) impairment, mitophagy dysregulation, defects biogenesis dynamics, well excessive ROS accumulation, with regards OP ( Figure 1 ). Furthermore, explore prospective strategies currently available for modulating ameliorate Undoubtedly, certain therapeutic still require investigation ensure their safety efficacy clinical treatments. However, perspective, potential establishing effective safe approaches osteoporosis appears promising.

Language: Английский

Citations

19

Mitochondrial diseases: from molecular mechanisms to therapeutic advances DOI Creative Commons
Hu Wen,

Hui Deng,

Bingyan Li

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2025, Volume and Issue: 10(1)

Published: Jan. 9, 2025

Abstract Mitochondria are essential for cellular function and viability, serving as central hubs of metabolism signaling. They possess various metabolic quality control mechanisms crucial maintaining normal activities. Mitochondrial genetic disorders can arise from a wide range mutations in either mitochondrial or nuclear DNA, which encode proteins other contents. These defects lead to breakdown metabolism, such the collapse oxidative phosphorylation, one mitochondria’s most critical functions. diseases, common group disorders, characterized by significant phenotypic heterogeneity. Clinical symptoms manifest systems organs throughout body, with differing degrees forms severity. The complexity relationship between mitochondria diseases results an inadequate understanding genotype-phenotype correlation these historically making diagnosis treatment challenging often leading unsatisfactory clinical outcomes. However, recent advancements research technology have significantly improved our management conditions. translations mitochondria-related therapies actively progressing. This review focuses on physiological mitochondria, pathogenesis potential diagnostic therapeutic applications. Additionally, this discusses future perspectives diseases.

Language: Английский

Citations

4

Proteomics analysis reveals age-related proteins in the urine of chronic kidney disease patients DOI Creative Commons
Lin Xiong, Changwei W. Wu, Sipei Chen

et al.

Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 11

Published: Jan. 6, 2025

Chronic kidney disease (CKD) is closely linked to the aging process, making identification of protein biomarkers that reflect in specific organs and tissues crucial for a deeper understanding this phenomenon. This study aimed identify potential aging-related proteins present urine CKD patients. Utilizing liquid chromatography-tandem mass spectrometry (LC-MS/MS) proteomic analysis, we identified total 1,712 samples from both healthy controls patients our discovery cohort. Among 845 overlapped, found 161 were associated with aging. By applying threshold p < 0.05 |log2 (fold change) | > 1.5, classified 114 as differentially expressed (DEPs). The analyzes conducted using Gene Ontology Kyoto Encyclopedia Genes Genomes revealed DEPs significantly enriched several clusters related In validation cohort, demonstrated exhibited lower urinary levels L-selectin (SELL), uromodulin (UMOD), epidermal growth factor (EGF). Additionally, significant negative correlation was between age EGF levels. estimated glomerular filtration rate (eGFR) showed positive SELL, UMOD, EGF, while 24-h proteinuria UMOD EGF. Furthermore, negatively correlated tubulointerstitial fibrosis, glomerulosclerosis. conclusion, emphasizes promise LC-MS/MS-based proteomics analysis identifying markers. Specifically, have been recognized promising indicators CKD.

Language: Английский

Citations

2

Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction—the trigger for PANoptosis in neurons DOI Creative Commons
Xiangyuan Meng, Qi Song, Zinan Liu

et al.

Frontiers in Aging Neuroscience, Journal Year: 2024, Volume and Issue: 16

Published: May 14, 2024

As the global population ages, incidence of elderly patients with dementia, represented by Alzheimer's disease (AD), will continue to increase. Previous studies have suggested that β-amyloid protein (Aβ) deposition is a key factor leading AD. However, clinical efficacy treating AD anti-Aβ antibodies not satisfactory, suggesting Aβ amyloidosis may be pathological change rather than Identification causes and development corresponding prevention treatment strategies an important goal current research. Following discovery soluble oligomeric forms (AβO) in 1998, scientists began focus on neurotoxicity AβOs. endogenous neurotoxin, active growth AβOs can lead neuronal death, which believed occur before plaque formation, are factors PANoptosis, newly proposed concept cell death includes known modes pyroptosis, apoptosis, necroptosis, form regulated PANoptosome complex. Neuronal survival depends proper mitochondrial function. Under conditions AβO interference, dysfunction occurs, releasing lethal contents as potential upstream effectors PANoptosome. Considering critical role neurons cognitive function well regulatory survival, investigation mechanisms PANoptosis crucial. This review describes disruption elucidates how activate causing during AD, providing guidance for targeted strategies.

Language: Английский

Citations

12

Cow placenta extract ameliorates d-galactose-induced liver damage by regulating BAX/CASP3 and p53/p21/p16 pathways DOI Creative Commons

Liuhong Shen,

Lei Fan, Hao Luo

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 323, P. 117685 - 117685

Published: Jan. 1, 2024

Placenta is a kind of traditional Chinese medicine, known as "Ziheche", which has the function tonifying qi and blood, nourishing liver kidney. extract (PE) been used for delaying organismal aging treating various diseases. Cow placenta rich natural resource with large mass. Its composition similar to that human placenta, but it not effectively utilized. However, little about effect CPE on mice.

Language: Английский

Citations

10

Enhancing healthy aging with small molecules: A mitochondrial perspective DOI

Xiujiao Qin,

Hongyuan Li, Huiying Zhao

et al.

Medicinal Research Reviews, Journal Year: 2024, Volume and Issue: 44(4), P. 1904 - 1922

Published: March 14, 2024

The pursuit of enhanced health during aging has prompted the exploration various strategies focused on reducing decline associated with process. A key area this is management mitochondrial dysfunction, a notable characteristic aging. This review sheds light crucial role that small molecules play in augmenting healthy aging, particularly through influencing functions. Mitochondrial oxidative damage, significant aspect can potentially be lessened interventions such as coenzyme Q10, alpha-lipoic acid, and variety antioxidants. Additionally, discusses approaches for enhancing proteostasis, emphasizing importance unfolded protein response inducers like doxycycline, agents affect mitophagy, urolithin A, spermidine, trehalose, taurine, which are vital sustaining quality control. Of equal methods modulating energy production, involve nicotinamide adenine dinucleotide boosters, adenosine 5'-monophosphate-activated kinase activators, compounds metformin mitochondria-targeted tamoxifen enhance metabolic function. Furthermore, delves into emerging encourage biogenesis. Together, these present promising avenue addressing age-related degradation, thereby setting stage development innovative treatment to meet extensive challenge.

Language: Английский

Citations

9

Mitochondria and the Repurposing of Diabetes Drugs for Off-Label Health Benefits DOI Open Access
Joyce Yip, Grace Shu Hui Chiang,

I Lee

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(1), P. 364 - 364

Published: Jan. 3, 2025

This review describes our current understanding of the role mitochondria in repurposing anti-diabetes drugs metformin, gliclazide, GLP-1 receptor agonists, and SGLT2 inhibitors for additional clinical benefits regarding unhealthy aging, long COVID, mental neurogenerative disorders, obesity. Metformin, most prominent these diabetes drugs, has been called “Drug Miracles Wonders,” as trials have found it to be beneficial human patients suffering from maladies. To promote viral replication all infected cells, SARS-CoV-2 stimulates liver cells produce glucose export into blood stream, which can cause COVID patients, reduces levels blood, was shown cut incidence rate half recovering SARS-CoV-2. Metformin leads phosphorylation AMP-activated protein kinase AMPK, accelerates import via transporter GLUT4 switches starvation mode, counteracting virus. Diabetes also stimulate unfolded response thus mitophagy, is healthy aging health. were mimic exercise help reduce body weight.

Language: Английский

Citations

1

Comprehensive bioinformatics analysis reveals novel potential biomarkers associated with aging and mitochondria in osteoporosis DOI Creative Commons
Ke Bi, Yuxi Chen,

Yuhang Hu

et al.

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

Published: Jan. 6, 2025

Osteoporosis (OP) is a prevalent age-related bone metabolic disease. Aging and mitochondrial dysfunction are involved in the onset progression of OP, but specific mechanisms have not been elucidated. The aim this study was to identify novel potential biomarkers associated with aging mitochondria OP. In study, based on GEO database, aging-related mitochondria-related differentially expressed genes (AR&MRDEGs) were screened. AR&MRDEGs enriched structure function. Then, 6 key identified by WGCNA multiple machine learning, diagnostic model constructed. efficacy validated using external datasets. results showed that had favorable prediction ability. Next, gene regulatory networks constructed single-gene GSEA analysis performed. addition, single-cell dataset from (scDEGs) identified. revealed (AR&MRGs) ERK pathway tissue stem cells (TSCs), membrane depolarization monocytes. Cellular communication TSCs active, numerous signaling interactions monocytes, macrophages immune cells. Finally, expression verified quantitative real-time PCR (qRT-PCR). This expected provide strategies for diagnosis treatment OP targeting mitochondria.

Language: Английский

Citations

1

Elucidating emerging signaling pathways driving endothelial dysfunction in cardiovascular aging DOI

Anna De Bartolo,

Tommaso Angelone, Carmine Rocca

et al.

Vascular Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 107462 - 107462

Published: Jan. 1, 2025

Language: Английский

Citations

1