KLF15 overexpression in myocytes fails to ameliorate ALS-related pathology or extend the lifespan of SOD1G93A mice

Massopust, Ryan; Juros, Devin; Shapiro, Dillon; Lopes, Mikayla; Haldar, Saptarsi M.; Taetzsch, Thomas; Valdez, Gregorio

doi:10.1016/j.nbd.2021.105583

Cited by 3 publications

(3 citation statements)

References 40 publications

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“…The effects of honokiol on alleviating glial cells activation might be a comprehensive result of the anti-inflammation capacity and anti-oxidant capacity. In addition, progressive degeneration of skeletal muscles is an early pathological feature of ALS which likely occurs prior to MNs in ALS patients and in the SOD1-G93A ALS mouse model 6 , 59 , 60 . Honokiol mitigated the group atrophy of the gastrocnemius muscle compared with the SOD1-G93A model mice.…”

Section: Discussionmentioning

confidence: 99%

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Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis

Zhou

Tang

Lan

et al. 2023

Acta Pharmaceutica Sinica B

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Section: Discussionmentioning

confidence: 99%

“…Although a number of candidates have been shown to delay disease progression in preclinical trials, riluzole and edaravone are only two drugs approved by US Food and Drug Administration for ALS treatment. However, their effects are limited and are only able to extend the survival by a few months 6 .…”

Section: Introductionmentioning

confidence: 99%

Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis

Zhou

Tang

Lan

et al. 2023

Acta Pharmaceutica Sinica B

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“…Those mice did not show any difference in disease progression or muscle atrophy compared to control animals. 67 These results demonstrate that an enhanced KLF15 expression is not capable to improve disease phenotypes, but rather an interplay of different proteins or down-and upstream targets is necessary to ameliorate disease progression. Besides this, KLF15 is involved in altered glucose metabolism which was described in ALS patients and mouse models.…”

Section: Discussionmentioning

confidence: 87%

Protein Network Analysis Reveals a Functional Connectivity of Dysregulated Processes in ALS and SMA

Kubinski

Claus²

2022

J Exp Neurosci

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Spinal Muscular Atrophy (SMA) and Amyotrophic Lateral Sclerosis (ALS) are neurodegenerative diseases which are characterized by the loss of motoneurons within the central nervous system. SMA is a monogenic disease caused by reduced levels of the Survival of motoneuron protein, whereas ALS is a multi-genic disease with over 50 identified disease-causing genes and involvement of environmental risk factors. Although these diseases have different causes, they partially share identical phenotypes and pathomechanisms. To analyze and identify functional connections and to get a global overview of altered pathways in both diseases, protein network analyses are commonly used. Here, we used an in silico tool to test for functional associations between proteins that are involved in actin cytoskeleton dynamics, fatty acid metabolism, skeletal muscle metabolism, stress granule dynamics as well as SMA or ALS risk factors, respectively. In network biology, interactions are represented by edges which connect proteins (nodes). Our approach showed that only a few edges are necessary to present a complex protein network of different biological processes. Moreover, Superoxide dismutase 1, which is mutated in ALS, and the actin-binding protein profilin1 play a central role in the connectivity of the aforementioned pathways. Our network indicates functional links between altered processes that are described in either ALS or SMA. These links may not have been considered in the past but represent putative targets to restore altered processes and reveal overlapping pathomechanisms in both diseases.

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Comprehensive analysis of next-generation sequencing data in COVID-19 and its secondary complications

Vastrad¹,

Vastrad²

2022

Preprint

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The ongoing pandemic of coronavirus disease 2019 (COVID-19) has made a serious public health threat globally. To discover key molecular changes in COVID-19 and its secondary complications, we analyzed next-generation sequencing (NGS) data of COVID-19. NGS data (GSE163151) was screened and downloaded from the Gene Expression Omnibus database (GEO). Differentially expressed genes (DEGs) were identified in the present study, using DESeq2 package in R programming software. Gene ontology (GO) and pathway enrichment analysis were performed, and the protein-protein interaction (PPI) network, module analysis, miRNA-hub gene regulatory network and TF-hub gene regulatory network were established. Subsequently, receiver operating characteristic curve (ROC) analysis was used to validate the diagonostics valuesof the hub genes. Firstly, 954 DEGs (477 up regulated and 477 down regulated) were identified from the four NGS dataset. GO enrichment analysis revealed enrichment of DEGs in genes related to the immune system process and multicellular organismal process, and REACTOME pathway enrichment analysis showed enrichment of DEGs in the immune system and formation of the cornified envelope. Hub genes were identified from the PPI network, module analysis, miRNA-hub gene regulatory network and TF-hub gene regulatory network. Furthermore, the ROC analysis indicate that COVID-19 and its secondary complications with following hub genes, namely, RPL10, FYN, FLNA, EEF1A1, UBA52, BMI1, ACTN2, CRMP1, TRIM42 and PTCH1, had good diagnostics values. This study identified several genes associated with COVID-19 and its secondary complications, which improves our knowledge of the disease mechanism.

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KLF15 overexpression in myocytes fails to ameliorate ALS-related pathology or extend the lifespan of SOD1G93A mice

Cited by 3 publications

References 40 publications

Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis

Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis

Protein Network Analysis Reveals a Functional Connectivity of Dysregulated Processes in ALS and SMA

Comprehensive analysis of next-generation sequencing data in COVID-19 and its secondary complications

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