Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury

Nishimura, Kenji; Taguchi, Kensei; Kishi, Seiji; Brooks, Craig R.; Ochi, Arisa; Kadoya, Hiroyuki; Ikeda, Yasumasa; Miyoshi, Masashi; Tamaki, Masanori; Abe, Hideharu; Aihara, Ken‐ichi; Kashihara, Naoki; Nagai, Kojiro

doi:10.1016/j.bbrc.2021.03.111

Cited by 10 publications

(8 citation statements)

References 29 publications

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“…The REG pathways were representative of the hallmarks of aging, including AMPK signaling and ubiquitination, lost oscillations in Old ( Figure 4A ). Of the pathways enriched solely in Aged, eNOS signaling likely reflects daily maintenance and homeostasis of the epithelium as well as renal hemodynamics 34 ( Figure 4B ). Finally, NAD + salvage pathways and acute immune responses were unique to Old, possibly as an adaptive mechanism to maintain homeostasis.…”

Section: Resultsmentioning

confidence: 99%

Defining the age-dependent and tissue-specific circadian transcriptome in male mice

et al. 2023

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Section: Resultsmentioning

confidence: 99%

Defining the age-dependent and tissue-specific circadian transcriptome in male mice

et al. 2023

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“…A previous study reported that the disruption of eNOS and ApoE genes accelerates kidney fibrosis and senescence after injury [ 37 ], indicating a protective role of the normal function of these genes. In addition, a meta-analysis that investigated the association between the ( eNOS ) 4b/a gene polymorphism and renal interstitial fibrosis in patients with DN demonstrated that the frequency of eNOS 4bb in DN renal interstitial patients was lower than that in non-nephropathy diabetic patients and normal controls [ 38 ].…”

Section: Resultsmentioning

confidence: 99%

Key Genetic Components of Fibrosis in Diabetic Nephropathy: An Updated Systematic Review and Meta-Analysis

Tziastoudi

Nikolaou

et al. 2022

IJMS

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Renal fibrosis (RF) constitutes the common end-point of all kinds of chronic kidney disease (CKD), regardless of the initial cause of disease. The aim of the present study was to identify the key players of fibrosis in the context of diabetic nephropathy (DN). A systematic review and meta-analysis of all available genetic association studies regarding the genes that are included in signaling pathways related to RF were performed. The evaluated studies were published in English and they were included in PubMed and the GWAS Catalog. After an extensive literature review and search of the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, eight signaling pathways related to RF were selected and all available genetic association studies of these genes were meta-analyzed. ACE, AGT, EDN1, EPO, FLT4, GREM1, IL1B, IL6, IL10, IL12RB1, NOS3, TGFB1, IGF2/INS/TH cluster, and VEGFA were highlighted as the key genetic components driving the fibrosis process in DN. The present systematic review and meta-analysis indicate, as key players of fibrosis in DN, sixteen genes. However, the results should be interpreted with caution because the number of studies was relatively small.

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“…The REG pathways were representative of the hallmarks of aging, including AMPK signaling and ubiquitination, lost oscillations in Old (Figure 4A). Of the pathways enriched solely in Aged, eNOS signaling likely reflects daily maintenance and homeostasis of the epithelium as well as renal hemodynamics (Nishimura et al, 2021) (Figure 4B). Finally, NAD + salvage pathways and acute immune responses were unique to Old, possibly as an adaptive mechanism to maintain homeostasis.…”

Section: Resultsmentioning

confidence: 99%

Defining the age-dependent and tissue-specific circadian transcriptome in male mice

Wolff

Gutierrez‐Monreal

Meng

et al. 2022

Preprint

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SUMMARYCellular circadian clocks direct a daily transcriptional program that supports homeostasis and resilience. Emerging evidence supports age-associated changes in circadian functions. To define age-dependent changes at the systems level, we profiled the circadian transcriptome in the hypothalamus, lung, heart, kidney, skeletal muscle, and adrenal gland in 3 age groups. We found age-dependent and tissue-specific clock output changes. Aging reduced the number of rhythmically expressed genes (REGs), indicative of weakened circadian control. Many genes gained rhythmicity in old tissues, reflecting an adaptive response. REGs were enriched for the hallmarks of aging, adding a new dimension to our understanding of aging. Differential gene expression analysis found that there were temporally distinct clusters of genes in tissue-specific manner. Increased daily gene expression variability is a common feature of aged tissues. This novel analysis extends the landscape of the understanding of aging and highlights the impact of aging on circadian clock function and temporal changes in gene expression.HIGHLIGHTS- Rhythmically expressed genes (REGs) in Young, but not Old mice, are enriched for the aging hallmarks across all tissues.- The numbers of REGs decline across all tissues with age implicating the circadian clock in altered homeostasis.- Age- and tissue-specific differentially expressed genes (DEGs) cluster at specific times of the day.- Increase in gene expression variability over a day is a common feature of aging tissues.

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Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury

Cited by 10 publications

References 29 publications

Defining the age-dependent and tissue-specific circadian transcriptome in male mice

Defining the age-dependent and tissue-specific circadian transcriptome in male mice

Key Genetic Components of Fibrosis in Diabetic Nephropathy: An Updated Systematic Review and Meta-Analysis

Defining the age-dependent and tissue-specific circadian transcriptome in male mice

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