Editorial: Look who’s talking: Dialogues with beta cells
The lives of cells are not solitary. Important elements of cell biology, such as function, differentiation, proliferation, and survival, are regulated through communication between cells located in separate organs and between cells of the same kind or distinct types within a tissue. Pancreatic beta...
| Autores: | , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2023 |
| País: | España |
| Institución: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositorio: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/309886 |
| Acceso en línea: | http://hdl.handle.net/10261/309886 |
| Access Level: | acceso abierto |
| Palabra clave: | Beta cell Crosstalk Communication Diabetes Islet |
| Sumario: | The lives of cells are not solitary. Important elements of cell biology, such as function, differentiation, proliferation, and survival, are regulated through communication between cells located in separate organs and between cells of the same kind or distinct types within a tissue. Pancreatic beta cells are regularly in communication with multiple cell types located within the islets of Langerhans as well as with cells outside the islets including cells of the exocrine pancreas, liver, muscle, adipose tissue, brain, or gut. These connections involve a variety of chemical and mechanical signals, are highly dynamic, and can tailor the behavior of beta cells in the short and long-term, ultimately contributing to the control of glucose homeostasis. Importantly, the types of communication and messages that they convey can change throughout the life of the organism. Thus, certain cell dialogues only take place during specific windows of time, i.e. embryogenesis or pregnancy, and mediate beta cell development and expansion under these physiological situations. On the other hand, some cell dialogues are forced upon pathological situations, such in the case of type 1 diabetes via the arrival of unexpected new neighbors of the immune system, or in the case of obesity via the reception of an unprecedented volume of signals from enlarged fat tissue. These latter dialogues often end in a difficult to resolve conflict that leads to beta cell dysfunction and/or loss and the onset of diabetes. A plethora of mouse models and cell lines have been generated in order to unravel the connection between pancreatic beta cells and other cells from various tissues aimed to identify key targets for diabetes treatment. Still, the identification of many mediators in such connections remains a challenge. |
|---|