Disturbance in the normal functions of the endoplasmic reticulum (ER) induces a signaling cascade that integrates adaptive and apoptotic responses. There are accumulating reports which demonstrate that prolonged ER stress results in the development and progression of metabolic diseases, including diabetes, obesity, fatty liver diseases, as well as many other diseases like neurodegenerative diseases, atherosclerosis, and cancer. ER protein homeostasis is tightly controlled by the integrated pathways including ER Associated Diseases (ERAD), Unfolded protein responses (UPR) and autophagy. Over-reaction or irremediable ER stress response often leads to cell death or senescence, while incompetent or failure in ER stress response will result in compromised ER or cellular function. Along with the recent progresses in mechanistic studies and therapeutic strategies, it is believed that targeting the ER homeostasis as well as stress response would be potential strategies for the treatment of various diseases driven by impaired ER function.
This Research Topic aims to:
1) provide cutting-edge knowledge on the regulatory mechanisms of ER homeostasis and stress response.
2) demonstrate novel connections between the physiological function of ER and metabolic disease pathogenesis, including obesity, hyperglycemia, hyperlipidemia, dysregulated hormone secretion, et.al., thus finally provide potential therapeutics against metabolic diseases through targeting ER function.
We welcome original basic and clinical research, case reports, review and mini review articles focusing on the following topics:
• ER stress response and its physiological function
• Novel pathways or mechanisms in ER stress response
• ER protein homeostasis
• ER homeostasis and endocrine cell function
• ER function in metabolic tissues
• ER homeostasis and obesity, diabetes, etc.
• Therapeutics against metabolic diseases targeting ER
• Other diseases related to ER dysfunction
Disturbance in the normal functions of the endoplasmic reticulum (ER) induces a signaling cascade that integrates adaptive and apoptotic responses. There are accumulating reports which demonstrate that prolonged ER stress results in the development and progression of metabolic diseases, including diabetes, obesity, fatty liver diseases, as well as many other diseases like neurodegenerative diseases, atherosclerosis, and cancer. ER protein homeostasis is tightly controlled by the integrated pathways including ER Associated Diseases (ERAD), Unfolded protein responses (UPR) and autophagy. Over-reaction or irremediable ER stress response often leads to cell death or senescence, while incompetent or failure in ER stress response will result in compromised ER or cellular function. Along with the recent progresses in mechanistic studies and therapeutic strategies, it is believed that targeting the ER homeostasis as well as stress response would be potential strategies for the treatment of various diseases driven by impaired ER function.
This Research Topic aims to:
1) provide cutting-edge knowledge on the regulatory mechanisms of ER homeostasis and stress response.
2) demonstrate novel connections between the physiological function of ER and metabolic disease pathogenesis, including obesity, hyperglycemia, hyperlipidemia, dysregulated hormone secretion, et.al., thus finally provide potential therapeutics against metabolic diseases through targeting ER function.
We welcome original basic and clinical research, case reports, review and mini review articles focusing on the following topics:
• ER stress response and its physiological function
• Novel pathways or mechanisms in ER stress response
• ER protein homeostasis
• ER homeostasis and endocrine cell function
• ER function in metabolic tissues
• ER homeostasis and obesity, diabetes, etc.
• Therapeutics against metabolic diseases targeting ER
• Other diseases related to ER dysfunction
