Mitochondrial Fission and Fusion: Molecular Mechanisms, Biological Functions, and Related Disorders

Ojaimi, Mode Al; Salah, Azza; El‐Hattab, Ayman W.

doi:10.3390/membranes12090893

Cited by 49 publications

(19 citation statements)

References 88 publications

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“…In addition, it has been suggested that inhibitors of human carbonic anhydrase 3reduce abnormal pain caused by neuropathy in mice (37,38). Human FBXL4, a protein associated with autosomal recessive, multisystemic mitochondrial disorders, also showed an upward trend in the experimental group (39,40), and studies have shown that elevated FBXL4 can cause chronic pain and inhibit its mediated TRAF2 expression (41).The levels of NADH-ubiquinone oxidoreductase chain 4L differ between the two groups.…”

Section: Discussionmentioning

confidence: 98%

Proteomics of long-term neurodevelopmental disorders of rats exposed to early pain stimulation in the neonatal period

Zuo

et al. 2023

Preprint

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Objective To screen the feasibility and value of quantitative proteomic tandem mass spectrometry labeling (TMT) technology for early pain stimulation leading to neurodevelopmental disorders during puberty in neonatal rats. Methods The rats were randomly divided into two groups at postnatal day one (P1), and the skin was pricked for seven consecutive days in the experimental group; the control group was stroked simultaneously. A Morris water maze experiment was performed at P45 and P48. The rats were sacrificed at P50, and the proteins extracted from the hippocampal tissues were analyzed by TMT quantitative proteomics. The differentially expressed proteins were identified as biologically relevant proteins after pain intervention. Results The Morris water maze experiment suggested that the experimental group of rats had a significantly longer escape latency at P45 and P48 than the control group (P<0.05). At P49, Rats in the experimental group crossed the traversing platform less often than the control group within 60 s. Hippocampal tissue proteomics analysis showed than 33 proteins were upregulated, and 37 were downregulated. The differentially expressed proteins were enriched in different GO subsets, the most significant of which were sucrose metabolic process, response to stilbenoid maltose metabolic process, disaccharide metabolic process, circulating immunoglobulin complex, haptoglobin-hemoglobin complex, hemoglobin complex, replisome, purine-rich negative regulatory element binding, biliverdin reductase activity, alpha-1,4-glucosidase activity, and retinal dehydrogenase activity. KEGG enrichment analysis was most significant for starch and sucrose metabolism, galactose metabolism, antigen processing and presentation, and TGF-beta signaling. The core proteins were identified by constructing protein interaction networks. Four essential differentially expressed proteins were screened, including microtubule-associated serine-/threonine-protein kinase, carbonic anhydrase 3, F-box and leucine-rich repeat protein 4, and NADH-ubiquinone oxidoreductase chain 4L. Conclusions TMT-labeled proteomics identified energy metabolic processes, developmental processes, cellular processes, bioregulation, and signaling as the main targets of distant neurodevelopmental disorders caused by painful stimulation. Microtubule-associated serine/threonine-protein kinase, carbonic anhydrase 3, F-box and leucine-rich repeat protein 4, and NADH-ubiquinone oxidoreductase chain 4L may be involved in the cognitive impairment of adolescence caused by early pain stimulation in neonatal rats.

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Section: Discussionmentioning

confidence: 98%

Proteomics of long-term neurodevelopmental disorders of rats exposed to early pain stimulation in the neonatal period

Zuo

et al. 2023

Preprint

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“…11,32 Mitochondrial fusion is regulated by three GTPase-dependent proteins, namely Mfn1 and Mfn2, which regulate outer membrane fusion, and OPA1, which regulates inner membrane fusion. Accumulating evidence indicates that deletion of Mfn1 and Mfn2 causes abnormal mitochondrial structure, 33,34 whereas Opa1 deletion mainly affects endosomal cristae formation, leading to impaired mitochondrial energy production. 35,36 Mitochondrial fission is mediated by Drp1, which oligomerically contracts and cleaves the mitochondrial membrane by binding to the ligand Fis1 of the outer mitochondrial membrane after phosphorylation at serine 616.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress induced by turbulence of mitochondrial fusion and fission was involved in stressed cardiomyocyte injury

Zhang,

Li,

Zhu

et al. 2023

J Cellular Molecular Medi

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Mitochondria are sensitive organelles that sense intrinsic and extrinsic stressors and maintain cellular physiological functions through the dynamic homeostasis of mitochondrial fusion and fission. Numerous pathological processes are associated with mitochondrial fusion and fission disorders. However, the molecular mechanism by which stress induces cardiac pathophysiological changes through destabilising mitochondrial fusion and fission is unclear. Therefore, this study aimed to investigate whether the endoplasmic reticulum stress signalling pathway initiated by the turbulence of mitochondrial fusion and fission under stressful circumstances is involved in cardiomyocyte damage. Based on the successful establishment of the classical stress rat model of restraint plus ice water swimming, we measured the content of serum lactate dehydrogenase. We used haematoxylin–eosin staining, special histochemical staining, RT‐qPCR and western blotting to clarify the cardiac pathology, ultrastructural changes and expression patterns of mitochondrial fusion and fission marker proteins and endoplasmic reticulum stress signalling pathway proteins. The results indicated that mitochondrial fusion and fission markers and proteins of the endoplasmic reticulum stress JNK signalling pathway showed significant abnormal dynamic changes with the prolongation of stress, and stabilisation of mitochondrial fusion and fission using Mdivi‐1 could effectively improve these abnormal expressions and ameliorate cardiomyocyte injury. These findings suggest that stress could contribute to pathological cardiac injury, closely linked to the endoplasmic reticulum stress JNK signalling pathway induced by mitochondrial fusion and fission turbulence.

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“…Mitochondrial self-regulation occurs through constant fission and fusion, providing energy for cellular homeostasis and regulating macroautophagy, calcium homeostasis, innate immunity, signaling and apoptosis. The relative balance of mitochondrial fission and fusion is essential to maintain the quality and function of mitochondria and is an important basis for normal cellular activity 7 , 39 . In contrast, mitophagy involves the sequestration and removal of damaged mitochondria from a cell through a specific autophagic pathway, thereby maintaining intracellular mitochondrial homeostasis 40 .…”

Section: Dynamic Regulation Of Mitochondriamentioning

confidence: 99%

The crosstalk between ferroptosis and mitochondrial dynamic regulatory networks

Li,

Jia,

Ding

et al. 2023

Int. J. Biol. Sci.

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Ferroptosis is an iron-driven cell death modality characterized by iron accumulation and excessive lipid peroxidation. Ferroptosis is closely related to mitochondrial function, as indicated by studies showing that mitochondrial dysfunction and damage promote oxidative stress, which in turn induces ferroptosis. Mitochondria play crucial roles in cellular homeostasis, and abnormalities in their morphology and function are closely associated with the development of many diseases. Mitochondria are highly dynamic organelles, and their stability is maintained through a series of regulatory pathways. Mitochondrial homeostasis is dynamically regulated, mainly via key processes such as mitochondrial fission, mitochondrial fusion and mitophagy; however, mitochondrial processes are prone to dysregulation. Mitochondrial fission and fusion and mitophagy are intimately related to ferroptosis. Therefore, investigations into the dynamic regulation of mitochondrial processes during ferroptosis are important to provide a better understanding of the development of disease. In this paper, we systematically summarized changes in ferroptosis, mitochondrial fission and fusion and mitophagy to promote an in-depth understanding of the mechanism underlying ferroptosis and provide a corresponding reference for the treatment of related diseases.

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Mitochondrial Fission and Fusion: Molecular Mechanisms, Biological Functions, and Related Disorders

Cited by 49 publications

References 88 publications

Proteomics of long-term neurodevelopmental disorders of rats exposed to early pain stimulation in the neonatal period

Proteomics of long-term neurodevelopmental disorders of rats exposed to early pain stimulation in the neonatal period

Endoplasmic reticulum stress induced by turbulence of mitochondrial fusion and fission was involved in stressed cardiomyocyte injury

The crosstalk between ferroptosis and mitochondrial dynamic regulatory networks

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