Research Topic

Stress Response in Islet β-cell Production and Function

About this Research Topic

All cells have developed intricate mechanisms to handle stress for sustained function and survival. These include oxidative stress responses that reduce the amount of reactive oxygen species and unfolded-protein responses to clear misfolded and unfolded proteins in both cytoplasm and organelles. These responses are particularly important for pancreatic islet beta cells, which secrete insulin to regulate glucose homeostasis. Intriguingly, both failure and overactivation of stress response can cause beta-cell dysfunction, loss of identity, and eventual death (i.e. β-cell failure). This consequently results in Type 2 diabetes (T2D), a disease that afflicts over 450 million people globally. Thus, understanding the regulation of stress response in beta cells is essential for stopping β-cell failure and T2D, with the past decade witnessing an explosion in literature that explore stress responses in beta-cell survival and function.

Goal: The overall goal of this Research Topic is to capture the current state of stress response studies in beta cells in the forms of Original Research, Review, and Mini Review articles.

Scope/Sub-areas:
• Stress response in beta-cell development
• Insulin biosynthesis/trafficking and generation of unfolded proinsulin
• Glucose metabolism and generation of reactive oxygen species
• The regulation and function of oxidative stress response
• The regulation and function of unfolded-protein responses, including in cytoplasm and organelles
• Inflammation and cellular stress responses
• The association/function of stress-response factors in human beta-cell function and diabetes
• Stress response as targets to restore beta-cell function


Keywords: Stress response, beta cells, insulin, diabetes, inflammation, unfolded-protein response, oxidative stress response, secretion, trafficking, endoplasmic reticulum, mitochondria, Bid, CHOP, PERK, IRE1, Atf6, HSF1, and Nurf2


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

All cells have developed intricate mechanisms to handle stress for sustained function and survival. These include oxidative stress responses that reduce the amount of reactive oxygen species and unfolded-protein responses to clear misfolded and unfolded proteins in both cytoplasm and organelles. These responses are particularly important for pancreatic islet beta cells, which secrete insulin to regulate glucose homeostasis. Intriguingly, both failure and overactivation of stress response can cause beta-cell dysfunction, loss of identity, and eventual death (i.e. β-cell failure). This consequently results in Type 2 diabetes (T2D), a disease that afflicts over 450 million people globally. Thus, understanding the regulation of stress response in beta cells is essential for stopping β-cell failure and T2D, with the past decade witnessing an explosion in literature that explore stress responses in beta-cell survival and function.

Goal: The overall goal of this Research Topic is to capture the current state of stress response studies in beta cells in the forms of Original Research, Review, and Mini Review articles.

Scope/Sub-areas:
• Stress response in beta-cell development
• Insulin biosynthesis/trafficking and generation of unfolded proinsulin
• Glucose metabolism and generation of reactive oxygen species
• The regulation and function of oxidative stress response
• The regulation and function of unfolded-protein responses, including in cytoplasm and organelles
• Inflammation and cellular stress responses
• The association/function of stress-response factors in human beta-cell function and diabetes
• Stress response as targets to restore beta-cell function


Keywords: Stress response, beta cells, insulin, diabetes, inflammation, unfolded-protein response, oxidative stress response, secretion, trafficking, endoplasmic reticulum, mitochondria, Bid, CHOP, PERK, IRE1, Atf6, HSF1, and Nurf2


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

19 March 2021 Abstract
31 May 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

19 March 2021 Abstract
31 May 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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