The concept of a ‘microenvironment’ has shaped our understanding of the pathogenesis of various diseases, especially tumorigenesis. However, different from the tumor, kidney lesions are not homogeneous across the kidney parenchyma amid disease progression. Instead, they initiate at a specific site to form a niche-like microenvironmental change after acute kidney injury or chronic fibrosis. A kidney local microenvironment after an injury is complex, heterotypic, and dynamic, comprising diverse cellular components such as injured tubular cells, activated fibroblasts, pericytes, inflammatory cells, endothelial cells, podocytes, and others, extracellular matrix, and a variety of secreted factors. The role of a microenvironment in the pathogenesis of kidney disease has largely been undetermined. Deeply exploring cell-cell communications or cell-matrix interactions in forming a kidney local microenvironment will be greatly beneficial for constructing a warning system to monitor disease progression and design novel therapeutic strategies to prevent or mitigate kidney diseases.
The overall goal of this Research Topic is to report the findings on the composition, structure, function, and regulation of a kidney local microenvironment after kidney diseases caused by a variety of etiologies.
Research publications will cover animal studies and human studies after acute kidney injury (AKI) or chronic kidney disease (CKD). We welcome the submission of Original Research and Reviews on the subtopics below:
• Cell-cell or cell-matrix communications in microenvironment formation after AKI or CKD
• Systems biology (e.g. multi-omics, mathematical modeling) in dissecting the microenvironment formation after AKI or CKD
• Therapeutic targeting the formation of microenvironment after AKI or CKD
• Kidney single-cell sequencing
• Spatial Imaging strategies
The concept of a ‘microenvironment’ has shaped our understanding of the pathogenesis of various diseases, especially tumorigenesis. However, different from the tumor, kidney lesions are not homogeneous across the kidney parenchyma amid disease progression. Instead, they initiate at a specific site to form a niche-like microenvironmental change after acute kidney injury or chronic fibrosis. A kidney local microenvironment after an injury is complex, heterotypic, and dynamic, comprising diverse cellular components such as injured tubular cells, activated fibroblasts, pericytes, inflammatory cells, endothelial cells, podocytes, and others, extracellular matrix, and a variety of secreted factors. The role of a microenvironment in the pathogenesis of kidney disease has largely been undetermined. Deeply exploring cell-cell communications or cell-matrix interactions in forming a kidney local microenvironment will be greatly beneficial for constructing a warning system to monitor disease progression and design novel therapeutic strategies to prevent or mitigate kidney diseases.
The overall goal of this Research Topic is to report the findings on the composition, structure, function, and regulation of a kidney local microenvironment after kidney diseases caused by a variety of etiologies.
Research publications will cover animal studies and human studies after acute kidney injury (AKI) or chronic kidney disease (CKD). We welcome the submission of Original Research and Reviews on the subtopics below:
• Cell-cell or cell-matrix communications in microenvironment formation after AKI or CKD
• Systems biology (e.g. multi-omics, mathematical modeling) in dissecting the microenvironment formation after AKI or CKD
• Therapeutic targeting the formation of microenvironment after AKI or CKD
• Kidney single-cell sequencing
• Spatial Imaging strategies
