Artemisia alleviates AGE-induced liver complications via MAPK and RAGE signaling pathways modulation: a combinatorial study

Moulahoum, Hichem; Ghorbanizamani, Faezeh; Khiari, Zineb; Toumi, M; Benazzoug, Yasmina; Tok, Kerem; Tımur, Suna; Zihnioğlu, Figen

doi:10.1007/s11010-022-04437-w

Cited by 6 publications

(4 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, the DEGs in the livers between treated with and without MnCl 2 on the 1st and 3rd day were involved in MAPK signaling pathway (Fig. 3A-B), which was consistent with previous observations [41][42][43]. Li et al (2021) found that LPS could cause the liver damage, and MAPK signaling pathways might be involved in LPS-induced hepatotoxicity in geese [41].…”

Section: Discussionsupporting

confidence: 92%

See 1 more Smart Citation

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Yang

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

Excessive exposure to manganese (Mn) can cause severe toxicity in human and animal organs, particularly the liver. However, the specific mechanisms of Mn-induced hepatotoxicity remain unclear. Thus, the objective of this study was to identify the key genes associated with hepatotoxicity caused by Mn administration. We obtained the gene expression data set GSE59923 from the Gene Expression Omnibus, which included liver samples treated with manganese chloride (MnCl2) as well as control samples. Through our analysis, we identified 222, 351, and 494 differentially expressed genes (DEGs) in the livers treated with MnCl2 at 700 mg/kg on the 1st, 3rd, and 5th day, respectively. Notably, we found a total of 27 overlapping DEGs in the liver samples. Biological process analysis revealed that these common DEGs were associated with the response to xenobiotic stimulus, cellular calcium ion homeostasis, and ion transmembrane transport. Pathway analysis further indicated the involvement of cAMP, p53, PI3K-Akt, MAPK, and AMPK signaling pathways in Mn-induced hepatotoxicity. Furthermore, we identified several important genes, including CCR2, CDKN1A, CELSR2, LCN2, and PER2, which appeared to play a role in Mn-induced hepatotoxicity. Taken together, this study sheds light on the molecular mechanisms underlying Mn-induced hepatotoxicity, contributing to our overall understanding of this condition.

show abstract

Section: Discussionsupporting

confidence: 92%

“…Similarly, MAPK signaling pathway participated in advanced glycation end-products-induced liver damages and oxidative stress. Moreover, it regulated oxidative stress markers (NO and lipid peroxidation), apoptosis (CASP3), and in ammatory mediators (IL-6 and TNF alpha) in liver damages [43].…”

Section: Discussionmentioning

confidence: 98%

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Yang

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…To find anti-aging therapeutic approaches at the cellular level by studying signaling networks deeply, DDR can be controlled by modulating telomere shortening via telomerase activation [169]. Therefore, identifying potential agents that act on telomeres shortening, novel anti-aging approaches can be introduced [170].…”

Section: Discussionmentioning

confidence: 99%

DNA damage response & senescence-associated secretory phenotype pathway: Emerging targets for anti-aging

Nadeem,

Parveen,

Kim

2023

Preprint

View full text Add to dashboard Cite

Cellular aging has drawn the attention of researchers, scientists, and biotech businesses for the treatment of a number of medical conditions. Cellular aging is primarily defined by consistent cessation of proliferative development in response to internal and external stressors, including DNA damage, telomere shortening, mitochondrial dysfunction, and regulation of the senescence-associated secretory phenotype (SASP). Disturbances involving these factors may contribute to age-related disease development. Therefore, the current review aims to explore anti-aging factors targeting DNA damage response and SASP regulation and their detailed signaling networks. In addition, it provides an opportunity for researchers to identify not only anti-aging targets, but also anti-aging therapeutic strategies based on identified and non-identified targets.

show abstract

“…Plant extracts derived from Artemisia herbalba were demonstrated to attenuate the production of pro-inflammatory cytokines, such as TNF-α and interleukin-6 (IL-6), which are formed through AGE–RAGE signaling pathways [ 67 ]. Polyphenols from tea also regulate the RAGE expression and thereby attenuate the MAPK and TGF-β signaling pathways [ 68 ].…”

Section: Receptors For Advanced Glycation Endproducts (Rage)mentioning

confidence: 99%

RAGE Inhibitors in Neurodegenerative Diseases

2023

View full text Add to dashboard Cite

Nonenzymatic reactions of reducing sugars with primary amino groups of amino acids, proteins, and nucleic acids, followed by oxidative degradations would lead to the formation of advanced glycation endproducts (AGEs). The AGEs exert multifactorial effects on cell damage leading to the onset of neurological disorders. The interaction of AGEs with the receptors for advanced glycation endproducts (RAGE) contribute to the activation of intracellular signaling and the expression of the pro-inflammatory transcription factors and various inflammatory cytokines. This inflammatory signaling cascade is associated with various neurological diseases, including Alzheimer’s disease (AD), secondary effects of traumatic brain injury (TBI), amyotrophic lateral sclerosis (ALS), and diabetic neuropathy, and other AGE-related diseases, including diabetes and atherosclerosis. Furthermore, the imbalance of gut microbiota and intestinal inflammation are also associated with endothelial dysfunction, disrupted blood–brain barrier (BBB) and thereby the onset and progression of AD and other neurological diseases. AGEs and RAGE play an important role in altering the gut microbiota composition and thereby increase the gut permeability and affect the modulation of the immune-related cytokines. The inhibition of the AGE–RAGE interactions, through small molecule-based therapeutics, prevents the inflammatory cascade of events associated with AGE–RAGE interactions, and thereby attenuates the disease progression. Some of the RAGE antagonists, such as Azeliragon, are currently in clinical development for treating neurological diseases, including AD, although currently there have been no FDA-approved therapeutics based on the RAGE antagonists. This review outlines the AGE–RAGE interactions as a leading cause of the onset of neurological diseases and the current efforts on developing therapeutics for neurological diseases based on the RAGE antagonists.

show abstract

Artemisia alleviates AGE-induced liver complications via MAPK and RAGE signaling pathways modulation: a combinatorial study

Cited by 6 publications

References 45 publications

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

DNA damage response & senescence-associated secretory phenotype pathway: Emerging targets for anti-aging

RAGE Inhibitors in Neurodegenerative Diseases

Contact Info

Product

Resources

About

Artemisia alleviates AGE-induced liver complications via MAPK and RAGE signaling pathways modulation: a combinatorial study

Cited by 6 publications

References 45 publications

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

DNA damage response &amp; senescence-associated secretory phenotype pathway: Emerging targets for anti-aging

RAGE Inhibitors in Neurodegenerative Diseases

Contact Info

Product

Resources

About

DNA damage response & senescence-associated secretory phenotype pathway: Emerging targets for anti-aging