With the incidence of type2 diabetes mellitus (T2DM) linked exponentially to ageing and obesity, the underlying role of chronic and sterile inflammation in pathogenesis and progression of its secondary complications has become well established. Whilst cross-sectional studies indicate a strong association between retinopathy and kidney outcomes in people with T2DM, people with diabetic nephropathy reportedly experienced higher incidence of eye disease compared to individuals without any diabetes related kidney issues. Collectively, these findings suggest a ‘common pathway’ indicative of general microvascular damage that, secondary to diabetes, leads to kidney dysfunction and loss of vision.
Although the precise role of inflammation in the development of diabetes and its secondary complications remains unclear, studies suggest that an accelerated ageing phenotype, coupled with a maladaptive immune response and aberrant cell communication underlie disease progression. Lack of understanding for how these factors develop and interrelate means that treatment of inflammation in diabetes, its complications and associated co-morbidities, represents an unmet clinical need. This Research Topic welcomes basic, translational, clinical, and applied research that improves our understanding of inflammation and disease progression in secondary complications of diabetes to include retinopathy, nephropathy, neuropathy, and cardiovascular disease. Original and/or review papers are encouraged. Potential areas of interest may include, but are not limited to:
1. The role of the innate immune response, e.g., NLRP3 inflammasome and downstream mediators.
2. Cell senescence and its Senescence Associated Secretory Phenotype (SASP).
3. Gap junction and hemichannel (connexins and/or pannexins) mediated cell communication.
4. The role and efficacy of innovative anti-inflammatory drugs e.g., senolytics, NLRP3 inhibitors, senomorphics, SGLT2 inhibitors, use of fecal microbiota transplants, etc.
Abstract submission is not mandatory, the Guest Editors encourage all interested researchers to submit their manuscript to the project even without submitting an abstract beforehand. In case you decide to submit an abstract, it does not have to coincide with the final abstract of your manuscript.
With the incidence of type2 diabetes mellitus (T2DM) linked exponentially to ageing and obesity, the underlying role of chronic and sterile inflammation in pathogenesis and progression of its secondary complications has become well established. Whilst cross-sectional studies indicate a strong association between retinopathy and kidney outcomes in people with T2DM, people with diabetic nephropathy reportedly experienced higher incidence of eye disease compared to individuals without any diabetes related kidney issues. Collectively, these findings suggest a ‘common pathway’ indicative of general microvascular damage that, secondary to diabetes, leads to kidney dysfunction and loss of vision.
Although the precise role of inflammation in the development of diabetes and its secondary complications remains unclear, studies suggest that an accelerated ageing phenotype, coupled with a maladaptive immune response and aberrant cell communication underlie disease progression. Lack of understanding for how these factors develop and interrelate means that treatment of inflammation in diabetes, its complications and associated co-morbidities, represents an unmet clinical need. This Research Topic welcomes basic, translational, clinical, and applied research that improves our understanding of inflammation and disease progression in secondary complications of diabetes to include retinopathy, nephropathy, neuropathy, and cardiovascular disease. Original and/or review papers are encouraged. Potential areas of interest may include, but are not limited to:
1. The role of the innate immune response, e.g., NLRP3 inflammasome and downstream mediators.
2. Cell senescence and its Senescence Associated Secretory Phenotype (SASP).
3. Gap junction and hemichannel (connexins and/or pannexins) mediated cell communication.
4. The role and efficacy of innovative anti-inflammatory drugs e.g., senolytics, NLRP3 inhibitors, senomorphics, SGLT2 inhibitors, use of fecal microbiota transplants, etc.
Abstract submission is not mandatory, the Guest Editors encourage all interested researchers to submit their manuscript to the project even without submitting an abstract beforehand. In case you decide to submit an abstract, it does not have to coincide with the final abstract of your manuscript.
