The increasing burden of endocrine diseases has accelerated the search for human glands. Cell death includes various forms, including apoptosis, necrosis, distension, scorching and autophagy. Most cell death of pathophysiological significance is necrotic, while normal metabolism is maintained by the apoptotic program. Endocrine cell death is subjected to pathophysiological processes such as autoimmune response, inflammation, insulin resistance, hyperglycemia/glucotoxicity and lipotoxicity, resulting in oxidative stress that contribute to dysfunction, dedifferentiation/ transdifferentiation, and death, which plays a causal role in the development and progression of metabolic diseases. Chronic hyperglycemia also stimulates inflammatory processes and pro-apoptotic mechanisms mediated by NO and NO-related species production, initiating a vicious cycle of death signal formation in multiple pathways. Thus, there may be several pathways by which cell death contributes to an improved endocrine profile. Recently, many efforts have been made to treat the deleterious effects of endocrine disorders, including drugs and inhibitors of anti-apoptotic effects. However, we are just beginning to understand the role of cell death in endocrine disorders. More research is needed to understand the numerous fundamentally unique features of the endocrine system. Also, a molecular understanding of cell death will help answer these open questions for the treatment of metabolic diseases and help develop new therapeutic strategies from this area of research.
With this in mind, we have opened this Research Topic to implement current knowledge on cell death related to endocrine diseases with a specific focus on the molecular mechanisms of disease onset and therapeutic targets. Potential topics include, but are not limited to the following:
- Identifying the molecular mechanisms of cell death in metabolic diseases;
- Regulation and function of anoikis;
- Study animal models of RCD (regulated cell death) in metabolic diseases;
- Identify the mechanisms of cell death related genes acting in metabolism;
We welcome submissions from all areas of molecular mechanisms and therapeutic targets of endocrine disease development, with a particular interest in works related to human cell death. Programmed responses in these diseases may provide new insights into metabolic signaling pathways, disease epigenetics, and the selectivity of biological traits. With the latest scientific breakthroughs in this field, our knowledge will increase exponentially, allowing us to unravel the mysteries of endocrinology even further.
The increasing burden of endocrine diseases has accelerated the search for human glands. Cell death includes various forms, including apoptosis, necrosis, distension, scorching and autophagy. Most cell death of pathophysiological significance is necrotic, while normal metabolism is maintained by the apoptotic program. Endocrine cell death is subjected to pathophysiological processes such as autoimmune response, inflammation, insulin resistance, hyperglycemia/glucotoxicity and lipotoxicity, resulting in oxidative stress that contribute to dysfunction, dedifferentiation/ transdifferentiation, and death, which plays a causal role in the development and progression of metabolic diseases. Chronic hyperglycemia also stimulates inflammatory processes and pro-apoptotic mechanisms mediated by NO and NO-related species production, initiating a vicious cycle of death signal formation in multiple pathways. Thus, there may be several pathways by which cell death contributes to an improved endocrine profile. Recently, many efforts have been made to treat the deleterious effects of endocrine disorders, including drugs and inhibitors of anti-apoptotic effects. However, we are just beginning to understand the role of cell death in endocrine disorders. More research is needed to understand the numerous fundamentally unique features of the endocrine system. Also, a molecular understanding of cell death will help answer these open questions for the treatment of metabolic diseases and help develop new therapeutic strategies from this area of research.
With this in mind, we have opened this Research Topic to implement current knowledge on cell death related to endocrine diseases with a specific focus on the molecular mechanisms of disease onset and therapeutic targets. Potential topics include, but are not limited to the following:
- Identifying the molecular mechanisms of cell death in metabolic diseases;
- Regulation and function of anoikis;
- Study animal models of RCD (regulated cell death) in metabolic diseases;
- Identify the mechanisms of cell death related genes acting in metabolism;
We welcome submissions from all areas of molecular mechanisms and therapeutic targets of endocrine disease development, with a particular interest in works related to human cell death. Programmed responses in these diseases may provide new insights into metabolic signaling pathways, disease epigenetics, and the selectivity of biological traits. With the latest scientific breakthroughs in this field, our knowledge will increase exponentially, allowing us to unravel the mysteries of endocrinology even further.
