Department of Pharmacy

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Author: search.filters.author.Majumder, SyamantakSubject: search.filters.subject.Chronic kidney disease (CKD)

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    Significance of LncRNAs in AKI-to-CKD transition: a therapeutic and diagnostic viewpoint
    (Elsevier, 2024-04) Gaikwad, Anil Bhanudas; Majumder, Syamantak
    Acute kidney injury to chronic kidney disease (AKI-to-CKD) transition is a complex intermingling of characteristics of both AKI and CKD. Pathophysiologically, the transition lasts seven days after the AKI episode and thereafter silently progresses towards CKD. Growing reports confirm that the AKI-to-CKD transition is heavily regulated by epigenetic modifiers. Long non-coding RNAs (lncRNAs) share a diverse role in gene regulation at transcriptional and translational levels and have been reported to be involved in the regulation and progression of AKI-to-CKD transition. Several lncRNAs have been considered potential biomarkers for diagnosing kidney disease, including AKI and CKD. Targeting lncRNAs gives a promising therapeutic strategy against kidney diseases. The primitive role of lncRNA in the progression of the AKI-to-CKD transition is yet to be fully understood. As known, the lncRNAs could be used as a biomarker and a therapeutic target to halt the CKD development and progression after AKI. This review aims to deepen our understanding of the current knowledge regarding the involvement of lncRNAs in the AKI-to-CKD transition. This review primarily discusses the role of lncRNAs and the change in their mechanisms during different stages of kidney disease, such as in AKI, AKI-to-CKD transition, and CKD. Further, we have discussed the potential diagnostic and pharmacological outcomes of targeting lncRNAs to prevent or slow the progression of AKI-to-CKD transition.
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    Novel dysregulated long non-coding RNAs in the acute kidney injury-to-chronic kidney diseases transition unraveled by transcriptomic analysis
    (The British Pharmacological Society, 2024-11) Gaikwad, Anil Bhanudas; Majumder, Syamantak
    Acute kidney injury (AKI)-to-chronic kidney disease (CKD) transition involves a complex pathomechanism, including inflammation, apoptosis, and fibrosis where long non-coding RNAs (lncRNAs) play a crucial role in their regulation. However, to date, only a few lncRNAs have been discovered to be involved in the AKI-to-CKD transition. Therefore, this study aims to investigate the dysregulated lncRNAs in the AKI-to-CKD transition in vitro and in vivo. To mimic AKI-to-CKD transition both in vivo and in vitro, bilateral ischemia-reperfusion (IR) kidney injury was performed in Wistar rats (male), and normal rat kidney epithelial cell (NRK52E) cells were treated with exogenous transforming growth factor-β1 (TGF-β1). Further processing and analysis of samples collected from these studies (e.g., biochemical, histopathology, immunofluorescence, and RNA isolation) were also performed, and transcriptomic analysis was performed to identify the dysregulated lncRNAs. Rats subjected to IR showed a significant increase in kidney injury markers (creatinine, blood urea nitrogen (BUN), kidney injury molecule-1(KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) along with altered cell morphology). Apoptosis, inflammation, and fibrosis markers were markedly increased during the AKI-to-CKD transition. Furthermore, transcriptomic analysis revealed 62 and 84 unregulated and 95 and 92 downregulated lncRNAs in vivo and in vitro, respectively. Additionally, functional enrichment analysis revealed their involvement in various pathways, including the tumor necrosis factor (TNF), wingless-related integration site (Wnt), and hypoxia-inducible factor-1 (HIF-1) signaling pathways. These identified dysregulated lncRNAs significantly contribute to AKI-to-CKD transition, and their knockin/out can aid in developing targeted therapeutic interventions against AKI-to-CKD transition.