PINK spots: diseased mitochondria prepare for mitophagy

Osman, Sara

doi:10.1038/s41594-022-00733-7

Cited by 3 publications

(3 citation statements)

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“…Then, Parkin ubiquitinates the proteins on the outer surface of the mitochondrial membrane. Fusion of autophagosome and lysosome can degrade the damaged mitochondrion, further relieving the damages induced by T-2 toxin exposure [ 37 ]. AMPK is a serine/threonine protein kinase that acts as an energy sensor in cells.…”

Section: Discussionmentioning

confidence: 99%

Expression Profiles of Long Non-Coding RNAs in the Articular Cartilage of Rats Exposed to T-2 Toxin

Yu,

Wang,

Luo

et al. 2023

IJMS

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T-2 toxin could induce bone damage. But there is no specific mechanism about the long non-coding RNAs (lncRNAs) involved in T-2 toxin-induced articular cartilage injury. In this study, 24 SD rats were randomly divided into a control group and a T-2 group, which were administered 4% absolute ethanol and 100 ng/g · bw/day of T-2 toxin, respectively. After treatment for 4 weeks, safranin O/fast green staining identified the pathological changes in the articular cartilage of rats, and immunofluorescence verified the autophagy level increase in the T-2 group. Total RNA was isolated, and high-throughput sequencing was performed. A total of 620 differentially expressed lncRNAs (DE-lncRNAs) were identified, and 326 target genes were predicted. Enrichment analyses showed that the target genes of DE-lncRNAs were enriched in the autophagy-related biological processes and pathways. According to the autophagy database, a total of 23 autophagy-related genes were identified, and five hub genes (Foxo3, Foxo1, Stk11, Hdac4, and Rela) were screened using the Maximal Clique Centrality algorithm. The Human Protein Atlas database indicated that Rela and Hdac4 proteins were highly expressed in the bone marrow tissue, while Foxo3, Foxo1, and Stk11 proteins were reduced. According to Enrichr, etoposide and diatrizoic acid were identified as the key drugs. The real-time quantitative PCR results were consistent with the RNA sequencing (RNA-Seq) results. These results suggested that autophagy was involved in the rat articular cartilage lesions induced by T-2 toxin. The lncRNAs of NONRATG014223.2, NONRATG012484.2, NONRATG021591.2, NONRATG024691.2, and NONRATG002808.2, and their target genes of Foxo3, Foxo1, Stk11, Hdac4, and Rela, respectively, were the key regulator factors of autophagy.

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Section: Discussionmentioning

confidence: 99%

Expression Profiles of Long Non-Coding RNAs in the Articular Cartilage of Rats Exposed to T-2 Toxin

Yu,

Wang,

Luo

et al. 2023

IJMS

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“…In addition to mtDNA damage, an increase in ROS level may induce defective mitophagy, thus dampening the selective removal of malfunctioning mitochondria [43,51]. The ubiquitin-proteasome pathway components E3-ubiquitin ligase Parkin and PTENinducible putative kinase 1 (PINK1) are involved in the mitophagic process and recognized as Parkinson's disease (PD)-linked enzymes [52,53].…”

Section: Mitochondrial Dysfunction Associated With Ros Generationmentioning

confidence: 99%

Extracellular Vesicles in Aging: An Emerging Hallmark?

Manni

Buratta

Pallotta

et al. 2023

Cells

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Extracellular vesicles (EVs) are membrane-enclosed particles secreted by cells and circulating in body fluids. Initially considered as a tool to dispose of unnecessary material, they are now considered an additional method to transmit cell signals. Aging is characterized by a progressive impairment of the physiological functions of tissues and organs. The causes of aging are complex and interconnected, but there is consensus that genomic instability, telomere erosion, epigenetic alteration, and defective proteostasis are primary hallmarks of the aging process. Recent studies have provided evidence that many of these primary stresses are associated with an increased release of EVs in cell models, able to spread senescence signals in the recipient cell. Additional investigations on the role of EVs during aging also demonstrated the great potential of EVs for the modulation of age-related phenotypes and for pro-rejuvenation therapies, potentially beneficial for many diseases associated with aging. Here we reviewed the current literature on EV secretion in senescent cell models and in old vs. young individual body fluids, as well as recent studies addressing the potential of EVs from different sources as an anti-aging tool. Although this is a recent field, the robust consensus on the altered EV release in aging suggests that altered EV secretion could be considered an emerging hallmark of aging.

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“…Mutations in the protein ubiquitin kinase PINK1 may lead to defective mitophagy in early-onset PD. PINK1 and the ubiquitin E3 ligase Parkin work together in mitophagy processes; defective versions of these proteins are unable to clear dysfunctional mitochondria, leading to a progressive loss of dopaminergic neurons and the progression of motor symptoms in PD [83]. Furthermore, the deposition of α-syn induces mitochondrial dysfunction and alterations in mitophagy, causing PINK1 accumulation in neurons [84].…”

Section: Alternative Molecular Targets For Neurodegeneration: Mitocho...mentioning

confidence: 99%

Exploring Molecular Targets for Mitochondrial Therapies in Neurodegenerative Diseases

Plascencia-Villa

Perry

2023

IJMS

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The progressive deterioration of function and structure of brain cells in neurodegenerative diseases is accompanied by mitochondrial dysfunction, affecting cellular metabolism, intracellular signaling, cell differentiation, morphogenesis, and the activation of programmed cell death. However, most of the efforts to develop therapies for Alzheimer’s and Parkinson’s disease have focused on restoring or maintaining the neurotransmitters in affected neurons, removing abnormal protein aggregates through immunotherapies, or simply treating symptomatology. However, none of these approaches to treating neurodegeneration can stop or reverse the disease other than by helping to maintain mental function and manage behavioral symptoms. Here, we discuss alternative molecular targets for neurodegeneration treatments that focus on mitochondrial functions, including regulation of calcium ion (Ca2+) transport, protein modification, regulation of glucose metabolism, antioxidants, metal chelators, vitamin supplementation, and mitochondrial transference to compromised neurons. After pre-clinical evaluation and studies in animal models, some of these therapeutic compounds have advanced to clinical trials and are expected to have positive outcomes in subjects with neurodegeneration. These mitochondria-targeted therapeutic agents are an alternative to established or conventional molecular targets that have shown limited effectiveness in treating neurodegenerative diseases.

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PINK spots: diseased mitochondria prepare for mitophagy

Cited by 3 publications

References 0 publications

Expression Profiles of Long Non-Coding RNAs in the Articular Cartilage of Rats Exposed to T-2 Toxin

Expression Profiles of Long Non-Coding RNAs in the Articular Cartilage of Rats Exposed to T-2 Toxin

Extracellular Vesicles in Aging: An Emerging Hallmark?

Exploring Molecular Targets for Mitochondrial Therapies in Neurodegenerative Diseases

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