Publications by authors named "Chieh Ming Liao"
Introduction: Even during physiologic aging, the kidney experiences a loss of mass and a progressive functional decline. This is clinically relevant as it leads to an increased risk of acute and chronic kidney disease. The kidney tubular system plays an important role in the underlying aging process, but the involved cellular mechanisms remain largely elusive.
View Article and Find Full Text PDFThe kidney is a complex organ, which consists of multiple components with highly diverse cell types. A detailed understanding of these cell types in health and disease is crucial for the future development of preventive and curative treatment strategies. In recent years, single-cell RNA sequencing (scRNAseq) and single-nucleus RNA sequencing (snRNAseq) technology has opened up completely new possibilities in investigating the variety of renal cell populations in physiological and pathological states.
View Article and Find Full Text PDFCellular senescence of renal tubular cells is associated with chronic diseases and age-related kidney disorders. Therapies to antagonize senescence are, therefore, explored as novel approaches in nephropathy. Exosomes derived from human mesenchymal stroma-/stem-like cells (MSC) entail the transfer of multiple bioactive molecules, exhibiting profound regenerative potential in various tissues, including therapeutic effects in kidney diseases.
View Article and Find Full Text PDFArticle Synopsis
- Cellular senescence is a state where cells stop dividing permanently, linked to aging and organ dysfunction, and while common immortalized cell lines don't show this, primary kidney cells from mice can be used for study.
- Research investigated how genetic variations among different mouse strains affect cellular senescence in primary tubular epithelial cells (PTEC), showing significant differences in senescence markers based on the strain.
- Results indicated that PTEC from WSB mice showed the highest senescence levels while 129S1 mice had the lowest, suggesting that genetic diversity impacts cellular aging, which is crucial for future experiments in this area.
Background: Expression of SerpinB2, a regulator of inflammatory processes, has been described in the context of macrophage activation and cellular senescence. Given that mechanisms for these processes interact and can shape kidney disease, it seems plausible that SerpinB2 might play a role in renal aging, injury, and repair.
Methods: We subjected SerpinB2 knockout mice to ischemia-reperfusion injury or unilateral ureteral obstruction.