Newsights of endoplasmic reticulum in hypoxia

Guan, Lu; Ge, Rili; Ma, Shuang

doi:10.1016/j.biopha.2024.116812

Biomedicine & Pharmacotherapy

2024

DOI: 10.1016/j.biopha.2024.116812

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Newsights of endoplasmic reticulum in hypoxia

Lu Guan,

Rili Ge,

Shuang Ma

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2024

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Cited by 3 publications

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Research Progress of Endoplasmic Reticulum Targeting Metal Complexes in Cancer Therapy

Xu,

Wu,

Zhu

et al. 2024

Drug Development Research

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The development of anticancer drugs that target different organelles has received extensive attention due to the characteristics of cancer recurrence, metastasis, and drug resistance. The endoplasmic reticulum (ER) is an important structure within the cell that is primarily responsible for protein synthesis, folding, modification, and transport and plays a crucial role in cell function and health. ER stress activation induces cancer cell apoptosis. New anticancer drugs with different anticancer mechanisms and selectivity can be designed because of redox activity, composition diversity, and metal complexes structure regulation. Over the past few decades, dozens of metal complexes have killed cancer cells through ER stress, showing powerful tumor‐suppressive effects. This review summarizes the progress of research on anticancer metallic drugs that induce ER stress over the past few years, which is expected to bring more breakthroughs in the field of medicine and life science.

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Research Progress of Endoplasmic Reticulum Targeting Metal Complexes in Cancer Therapy

Xu,

Wu,

Zhu

et al. 2024

Drug Development Research

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Endoplasmic reticulum stress in acute lung injury and pulmonary fibrosis

Sun,

He,

Meng

et al. 2024

The FASEB Journal

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Pulmonary fibrosis (PF) is a progressive and irreversible lung disease that leads to diminished lung function, respiratory failure, and ultimately death and typically has a poor prognosis, with an average survival time of 2 to 5 years. Related articles suggested that endoplasmic reticulum (ER) stress played a critical role in the occurrence and progression of PF. The ER is responsible for maintaining protein homeostasis. However, factors such as aging, hypoxia, oxidative stress, or inflammation can disrupt this balance, promoting the accumulation of misfolded proteins in the ER and triggering ER stress. To cope with this situation, cells activate the unfolded protein response (UPR). Since acute lung injury (ALI) is one of the key onset events of PF, in this review, we will discuss the role of ER stress in ALI and PF by activating multiple signaling pathways and molecular mechanisms that affect the function and behavior of different cell types, with a focus on epithelial cells, fibroblasts, and macrophages. Linking ER stress to these cell types may broaden our understanding of the mechanisms underlying lung fibrosis and help us target these cells through these mechanisms. The relationship between ER stress and PF is still evolving, and future research will explore new strategies to regulate UPR pathways, providing novel therapeutic targets.

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HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis

Zou,

Yu,

Ruan

et al. 2024

Lupus Sci Med

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ObjectiveThe current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-β) in lupus nephritis (LN) by investigating its modulation of the Derlin-1/valosin-containing protein (VCP)/VCP-interacting membrane selenoprotein (VIMP) complex, endoplasmic reticulum (ER) stress and podocyte apoptosis.MethodsIn vitro and in vivo models of LN were established using glomerular podocytes treated with LN serum and MRL/lpr mice, respectively. The expression levels of HNF1-β were analysed in kidney tissues from patients with LN and MRL/lpr mice. To assess the effects of HNF1-β inhibition, an adeno-associated virus vector carrying HNF1-β short hairpin was administered to MRL/lpr mice. In vitro, glomerular podocytes were transfected with HNF1-β small interfering RNA (siRNA) or HNF1-β overexpression plasmids to explore their regulatory effects on the Derlin-1/VCP/VIMP complex and podocyte apoptosis. Dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays were performed to investigate the transcriptional activation of Derlin-1 and VCP promoters by HNF1-β.ResultsA significant decrease in HNF1-β levels was observed in kidney tissues from patients with LN while MRL/lpr mice exhibited an initial compensatory increase followed by a subsequent decrease in renal HNF1-β expression. Overexpression of HNF1-β transcriptionally upregulated Derlin-1 and VCP mitigating LN serum-induced ER stress and podocyte apoptosis. In contrast, HNF1-β inhibition exacerbated renal dysfunction and structural damage in MRL/lpr mice. Interestingly, HNF1-β inhibition transcriptionally repressed ERP44, leading to calcium ions (Ca²+) release-mediated disruption and inactivation of the Derlin-1/VCP/VIMP complex. This finding suggests that HNF1-β not only regulates the expression of key proteins in the Derlin-1/VCP/VIMP complex but also influences their assembly through Ca²+release regulation.ConclusionThis study provides novel insights into the regulatory mechanisms of HNF1-β in LN emphasising its impact on the Derlin-1/VCP/VIMP complex, ER stress and podocyte apoptosis. These findings have the potential to inform the development of new diagnostic tools and therapeutic strategies for LN.

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Newsights of endoplasmic reticulum in hypoxia

Cited by 3 publications

References 207 publications

Research Progress of Endoplasmic Reticulum Targeting Metal Complexes in Cancer Therapy

Research Progress of Endoplasmic Reticulum Targeting Metal Complexes in Cancer Therapy

Endoplasmic reticulum stress in acute lung injury and pulmonary fibrosis

HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis

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