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ER stress in obesity pathogenesis and management

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TLDR
In this article , the role of endoplasmic reticulum (ER) stress and the ER stress response in the onset and development of obesity was discussed, with a view to identifying novel therapeutic strategies for obesity prevention and management.
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This article is published in Trends in Pharmacological Sciences.The article was published on 2022-02-01 and is currently open access. It has received 21 citations till now. The article focuses on the topics: Obesity & Unfolded protein response.

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ER stress and UPR in Alzheimer’s disease: mechanisms, pathogenesis, treatments

TL;DR: In this paper , the unique role of endoplasmic reticulum (ER) stress in AD pathogenesis was analyzed and a thorough elucidation of ER stress machinery in AD pathology may help to open up new therapeutic avenues in the management of this devastating condition.
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New Insights Into the Interplay Among Autophagy, the NLRP3 Inflammasome and Inflammation in Adipose Tissue

Liyuan Zhu, +1 more
TL;DR: This work summarizes the current studies and potential mechanisms associated with autophagy and NLRP3 inflammasome in AT inflammation and aims to provide further evidence for research on obesity and obesity-related complications.
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Epigenetic modification in alcohol‐related liver diseases

TL;DR: Key findings to decipher AIEM and its role in the onset and development of ARLD and ALD are summarized from the perspectives of both cellular and animal models of alcohol exposure.
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ER stress and inflammation crosstalk in obesity

TL;DR: Key mechanisms of ER stress-induced inflammation in the context of obesity are elucidated and potential therapeutic strategies in the management of obesity through maneuvering ER stress and ER Stress-associated inflammation are summarized.
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PDIA4, a novel ER stress chaperone, modulates adiponectin expression and inflammation in adipose tissue

TL;DR: This is the first study demonstrating that PDIA4 modulates adipocytes by downregulating adiponectin, and metformin may serve as a potential therapeutic for preventing obesity viaPDIA4‐targeting.
References
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Journal ArticleDOI

Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes

TL;DR: It is shown that obesity causes endoplasmic reticulum (ER) stress, which leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptors substrate–1 (IRS-1).
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Chemical chaperones reduce ER stress and restore glucose homeostasis in a mouse model of type 2 diabetes.

TL;DR: It is demonstrated that chemical chaperones enhance the adaptive capacity of the ER and act as potent antidiabetic modalities with potential application in the treatment of type 2 diabetes.
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Hypothalamic IKKβ/NF-κB and ER Stress Link Overnutrition to Energy Imbalance and Obesity

TL;DR: The results show that the hypothalamic IKKbeta/NF-kappaB program is a general neural mechanism for energy imbalance underlying obesity and suggest that suppression of IKK beta either broadly across the brain or locally within the mediobasal hypothalamus, or specifically in hypothalamic AGRP neurons significantly protects against obesity and glucose intolerance.
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Defective hepatic autophagy in obesity promotes ER stress and causes insulin resistance.

TL;DR: The data demonstrate that autophagy is an important regulator of organelle function and insulin signaling and that loss of autophile is a critical component of defective insulin action seen in obesity.
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Mechanisms, regulation and functions of the unfolded protein response.

TL;DR: The unfolded protein response comprises a network of signalling pathways that reprogramme transcription, translation and protein modifications to relieve the load of unfolded or misfolded proteins in the endoplasmic reticulum lumen and restore proteostasis.
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