A Review of Traditional Chinese Medicine in Treating Renal Interstitial Fibrosis via Endoplasmic Reticulum Stress-Mediated Apoptosis

Liu, Yu; Chen, Dan-Qian; Han, Jingxue; Zhao, Tingting; Shu-ju, LI

doi:10.1155/2021/6667791

Cited by 3 publications

(3 citation statements)

References 88 publications

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“…In addition, the anti-renal fibrosis effects of some traditional Chinese formulas (such as Dahuang Fuzi Decoction [ 83 ], Fuzheng Huayu Recipe [ 84 ], Kangxianling [ 85 ], etc.) have been proven and might provide a viable approach for treating AAN as well as CKD induced by other causes [ 86 ]. Furthermore, the anti-fibrotic and regenerative effects of mesenchymal stem cells and their extracellular vesicles have been attested in animal models of AAN [ 87 , 88 ].…”

Section: Managementmentioning

confidence: 99%

Overview of aristolochic acid nephropathy: an update

Zhou,

Jiang,

et al. 2023

Kidney Res Clin Pract

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Aristolochic acid nephropathy (AAN) is a rapidly progressive renal interstitial fibrosis caused by medical or environmental exposure to aristolochic acid (AA). Since the outbreak of AAN in Belgium was reported nearly 30 years ago, the safety of herbal remedies has drawn considerable attention, and AAN has become a global public health problem. Breakthroughs have been made to better understand the disease, including the toxicity of AAs, the possible mechanisms of AAN, the disease patterns, and the pathological features; however, some critical problems remain unresolved. Because of the insidious onset of the disease, the incidence of AAN and the prevalence of exposure to AAs are unknown and might be largely underestimated. During the past decades, AA-containing herbs have been strictly administrated in many regions and the occurrence of AAN has declined sharply, yet cases of AAN are still sporadically reported. Despite the progress in the understanding of the disease’s pathogenesis, there is no effective treatment for delaying or reversing the renal deterioration caused by AAN. Therefore, the risk of exposure to AAs should be taken seriously by public health workers and clinicians. In this review, we updated the latest data on AAN, summarized the advances throughout these years, and put forward some challenges for future research.

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Section: Managementmentioning

confidence: 99%

Overview of aristolochic acid nephropathy: an update

Zhou,

Jiang,

et al. 2023

Kidney Res Clin Pract

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“…When a signal changes, it must trigger a series of signal changes, suppression or assistance (23). Additionally, sustained ER stress can induce other signaling pathways, such as DNA damage signaling and death receptor-mediated signaling, to promote cell apoptosis (24). The PERK-elF2α-ATF4-DNA damage inducible transcript 3 (GADD153) signaling pathway is one of the classic signaling pathways of ER stress (25).…”

Section: Role Of Er Stress In Cell Survival and Deathmentioning

confidence: 99%

Endoplasmic reticulum stress‑induced cell death as a potential mechanism for targeted therapy in glioblastoma (Review)

Shi

Zhang

et al. 2021

Int J Oncol

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The endoplasmic reticulum (ER) is an essential organelle for protein synthesis, folding and modification, lipid synthesis, and calcium storage. When endogenous or exogenous stimuli lead to ER-synthesized protein folding dysfunction, numerous unfolded or misfolded proteins accumulate in the ER cavity and cause a series of subsequent responses, referred to as ER stress. If ER stress is continuous, the unfolded protein response (UPR) is not enough to remove the accumulated unfolded and misfolded proteins, and thus, UPR signaling pathways will drive cell apoptosis. Glioblastoma (GBM) is currently the most aggressive and common malignant tumor of the nervous system. Since ER stress may increase the sensitivity of GBM to temozolomide, this article reviews the possible mechanisms of ER stress-induced apoptosis and the factors affecting ER stress, and evaluates the potential of ER stress as a therapeutic target.

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“…Numerous studies have con rmed that DDIT3-mediated apoptosis is involved in many human diseases, such as neurodegenerative diseases, diabetes, and metabolic diseases (Liu Y et al 2021 ). However, it is undeniable that DDIT3 is a double-edged sword, serving as both a cell death mechanism and a factor that can prolong tumor survival time.…”

Section: Introductionmentioning

confidence: 99%

The effect of DDIT3 on luminal A type breast cancer

Huang,

Xue,

Cao

2023

Preprint

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Purpose: To analyze the phenotypic changes of breast cancer (BC) cell before and after DDIT3 knockdown/overexpression, and preliminarily explore the regulatory mechanism. Also, to analyze the relationship between DDIT3 and prognosis by combining with bioinformatics methods, which provide a basis for further research on DDIT3 targeted treatment of BC. Methods: Loss- and gain-of-function studies, DDIT3 in MCF-7 (luminal A), and RNA-seq analysis were employed to investigate the functional impact of DDIT3 on BC cell proliferation and drug resistance. The relationship between DDIT3 and the prognosis of BC patients was systematically assessed using the tissue microarray technique along with qRT-PCR and publicly available data. Results: Survival analysis showed that patients with lower DDIT3 expression in luminal A type BC or BC patient which were undergoing endocrine therapy had a poorer prognosis, and DDIT3 expression was associated with overall survival (OS) significant. Following the knockdown of DDIT3 in MCF-7 cells, the proliferation rate was significantly increased, and drug resistance ability was just reversed. On the contrary, overexpression of DDIT3 had a relative inhibitory effect on target cell proliferation. Notably, the inhibition of DDIT3 expression upregulated TP63 and downregulated PDGFR, with the results being exactly opposite after the overexpression of DDIT3. Conclusion: These results have revealed that DDIT3 plays a critical role in luminal A type BC cell proliferation and TAM resistance, and it holds potential prognostic value in BC. Overall, DDIT3 may exert its functions in luminal A type BC by modulating the expression of TP63 and PDGFR.

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A Review of Traditional Chinese Medicine in Treating Renal Interstitial Fibrosis via Endoplasmic Reticulum Stress-Mediated Apoptosis

Cited by 3 publications

References 88 publications

Overview of aristolochic acid nephropathy: an update

Overview of aristolochic acid nephropathy: an update

Endoplasmic reticulum stress‑induced cell death as a potential mechanism for targeted therapy in glioblastoma (Review)

The effect of DDIT3 on luminal A type breast cancer

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