Current Status of Endoplasmic Reticulum Stress in Type II Diabetes

Mustapha, Sagir; Mohammed, Mustapha; Azemi, Ahmad Khusairi; Jatau, Abubakar Ibrahim; Shehu, Aishatu; Mustapha, Lukman; Aliyu, Ibrahim Muazzamu; Danraka, Rabi’u Nuhu; Amin, Abdulbasit; Bala, Auwal Adam; Ahmad, Wan Amir Nizam Wan; Rasool, Aida Hanum Ghulam; Mustafa, Mohd Rais; Mokhtar, Siti Safiah

doi:10.3390/molecules26144362

Cited by 22 publications

(10 citation statements)

References 111 publications

(130 reference statements)

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“…One of the key dysfunction processes in T2D, also identified in our enrichment analysis, is the UPR, which results from pro-insulin synthesis rate that exceeds the protein processing capacity of cells, leading to beta-cell dysfunction and death 82 , 83 . Thus, we compared scores of enriched GPs associated with UPR and protein synthesis and processing across individual cells (Fig.…”

Section: Resultsmentioning

confidence: 89%

Biologically informed deep learning to query gene programs in single-cell atlases

et al. 2023

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The increasing availability of large-scale single-cell atlases has enabled the detailed description of cell states. In parallel, advances in deep learning allow rapid analysis of newly generated query datasets by mapping them into reference atlases. However, existing data transformations learned to map query data are not easily explainable using biologically known concepts such as genes or pathways. Here we propose expiMap, a biologically informed deep-learning architecture that enables single-cell reference mapping. ExpiMap learns to map cells into biologically understandable components representing known ‘gene programs’. The activity of each cell for a gene program is learned while simultaneously refining them and learning de novo programs. We show that expiMap compares favourably to existing methods while bringing an additional layer of interpretability to integrative single-cell analysis. Furthermore, we demonstrate its applicability to analyse single-cell perturbation responses in different tissues and species and resolve responses of patients who have coronavirus disease 2019 to different treatments across cell types.

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Section: Resultsmentioning

confidence: 89%

Biologically informed deep learning to query gene programs in single-cell atlases

et al. 2023

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“…The mechanism involved in the Bixin antitumor effects has not been clearly elucidated. Physiological or pathological stresses can lead to disturbances in the normal protein folding ER functions, thereby causing ER stress [ 25 ]. It can induce the expression of the glucose-regulated proteins GRP78, GRP94, and other endoplasmic reticulum chaperones to produce a protective effect [ 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…Physiological or pathological stresses can lead to disturbances in the normal protein folding ER functions, thereby causing ER stress [ 25 ]. It can induce the expression of the glucose-regulated proteins GRP78, GRP94, and other endoplasmic reticulum chaperones to produce a protective effect [ 25 , 26 ]. In addition, ER stress can also independently induce cell cycle arrest and endogenous apoptosis [ 27 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

Bixin Prevents Colorectal Cancer Development through AMPK-Activated Endoplasmic Reticulum Stress

Qiu

Chang-feng

Zhang

2022

BioMed Research International

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Chemicals isolated from natural products have been broadly applied in the treatment of colorectal cancer (CRC). Bixin, an apocarotenoid from the seeds of Bixa orellana, exerts multiple pharmacological properties, including neuroprotective, anti-inflammatory, cardioprotective, and antitumor effects; yet, the therapeutic effects of Bixin on CRC are still unknown. Here, we described that Bixin treatment significantly inhibited the proliferation and motility of two CRC cell lines (CaCO2 and SW480) in vitro and in vivo. In addition, Bixin administration has sensitized CRC cells to TNF-related apoptosis-inducing ligand- (TRAIL-) induced cell apoptosis. Moreover, we showed that Bixin treatment initiated the activation of PERK/eIF-2α signal in CaCO2 and SW480 cells, leading to endoplasmic reticulum stress-associated apoptosis. Pharmacological inhibition of AMP-activated protein kinase (AMPK) abrogated the Bixin-induced activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2 alpha (eIF-2α) pathway, as well as reversed the inhibitory effects of Bixin on CRC development. In conclusion, this study indicated that Bixin treatment inhibits the progression of CRC through activating the AMPK/PERK/eIF-2α pathway, providing a novel potential strategy for clinical prevention of CRC.

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“…Indeed, multiple studies have demonstrated the involvement of UPR in the development and progression of metabolic diseases (for a review, see [ 47 ]). Thus, nowadays, it is known that ER stress participates in the impairment of insulin secretion and action; furthermore, ER stress has also been related to the development of degenerative complications (for a review, see [ 48 , 49 , 50 ]).…”

Section: Endoplasmic Reticulum Stress (Er Stress) and Inflammation In Dmmentioning

confidence: 99%

AGEs-Induced and Endoplasmic Reticulum Stress/Inflammation-Mediated Regulation of GLUT4 Expression and Atherogenesis in Diabetes Mellitus

Passarelli

Machado

2021

Cells

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In recent decades, complex and exquisite pathways involved in the endoplasmic reticulum (ER) and inflammatory stress responses have been demonstrated to participate in the development and progression of numerous diseases, among them diabetes mellitus (DM). In those pathways, several players participate in both, reflecting a complicated interplay between ER and inflammatory stress. In DM, ER and inflammatory stress are involved in both the pathogenesis of the loss of glycemic control and the development of degenerative complications. Furthermore, hyperglycemia increases the generation of advanced glycation end products (AGEs), which in turn refeed ER and inflammatory stress, contributing to worsening glycemic homeostasis and to accelerating the development of DM complications. In this review, we present the current knowledge regarding AGEs-induced and ER/inflammation-mediated regulation of the expression of GLUT4 (solute carrier family 2, facilitated glucose transporter member 4), as a marker of glycemic homeostasis and of cardiovascular disease (CVD) development/progression, as a leading cause of morbidity and mortality in DM.

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Current Status of Endoplasmic Reticulum Stress in Type II Diabetes

Cited by 22 publications

References 111 publications

Biologically informed deep learning to query gene programs in single-cell atlases

Biologically informed deep learning to query gene programs in single-cell atlases

Bixin Prevents Colorectal Cancer Development through AMPK-Activated Endoplasmic Reticulum Stress

AGEs-Induced and Endoplasmic Reticulum Stress/Inflammation-Mediated Regulation of GLUT4 Expression and Atherogenesis in Diabetes Mellitus

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