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About this Research Topic

Manuscript Submission Deadline 13 January 2023
Manuscript Extension Submission Deadline 12 February 2023

Diabetic cardiomyopathy (DCM) is evidenced by cardiac remodeling and cardiac dysfunction. Multiple mechanisms contribute to the development of DCM. Among the regulatory mechanisms, extracellular communications are gaining much attention for enhancing cardiomyocyte survival, recovering endothelial permeability, and inhibiting extracellular remodeling, etc., which are prominent pathological changes of DCM. Accumulating evidence have demonstrated that extracellular vesicles (EVs) mediated cells/tissues/organs communications are involved in the development of DCM. Investigation of the pathophysiology of extracellular communications may provide new opportunities in diagnosing and combatting DCM.

In this Research Topic, we would like to create a forum regarding the novel effects of extracellular communications in DCM. EV-mediated cross-talk between organs/tissues/cells will be investigated as well as the relevant mechanisms. The information may help better understand the pathophysiology of DCM and develop new therapeutic strategies combating against DCM.

We welcome submissions on the following topics, but are not limited to:
- Roles of organs/tissues/cells communication in DCM
- EVs modification strategies for cardiomyocyte targeting in DCM
- Role of EVs as biomarkers in the diagnosis of DCM
- Mechanisms of EVs assembly and loading in DCM
- Specific EV surface molecules and their interaction with target cells in DCM

Keywords: extracellular communications, extracellular vesicles, heart failure, cardiac dysfunction, diabetic cardiomyopathy


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.

Diabetic cardiomyopathy (DCM) is evidenced by cardiac remodeling and cardiac dysfunction. Multiple mechanisms contribute to the development of DCM. Among the regulatory mechanisms, extracellular communications are gaining much attention for enhancing cardiomyocyte survival, recovering endothelial permeability, and inhibiting extracellular remodeling, etc., which are prominent pathological changes of DCM. Accumulating evidence have demonstrated that extracellular vesicles (EVs) mediated cells/tissues/organs communications are involved in the development of DCM. Investigation of the pathophysiology of extracellular communications may provide new opportunities in diagnosing and combatting DCM.

In this Research Topic, we would like to create a forum regarding the novel effects of extracellular communications in DCM. EV-mediated cross-talk between organs/tissues/cells will be investigated as well as the relevant mechanisms. The information may help better understand the pathophysiology of DCM and develop new therapeutic strategies combating against DCM.

We welcome submissions on the following topics, but are not limited to:
- Roles of organs/tissues/cells communication in DCM
- EVs modification strategies for cardiomyocyte targeting in DCM
- Role of EVs as biomarkers in the diagnosis of DCM
- Mechanisms of EVs assembly and loading in DCM
- Specific EV surface molecules and their interaction with target cells in DCM

Keywords: extracellular communications, extracellular vesicles, heart failure, cardiac dysfunction, diabetic cardiomyopathy


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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