3 results match your criteria: "USA. Electronic address: agreka@broadinstitute.org.[Affiliation]"
Protective role for kidney TREM2 macrophages in obesity- and diabetes-induced kidney injury.
Cell Rep
June 2024
Broad Institute of MIT and Harvard, Cambridge, MA, USA; Kidney Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address:
Article Synopsis
- - Diabetic kidney disease (DKD) is a major cause of kidney failure linked to diabetes and obesity, but effective treatments to slow its progression are currently unavailable.
- - Research on single-cell transcriptomic profiles from DKD patients and mouse models reveals a growing population of macrophages expressing TREM2 in mice fed a high-fat diet, which correlates with obesity and diabetes.
- - In mice lacking TREM2, increased kidney damage and cell injury were observed, indicating that boosting TREM2 macrophages could be a promising therapeutic approach for DKD.
Charting a TRP to Novel Therapeutic Destinations for Kidney Diseases.
Trends Pharmacol Sci
December 2019
Broad Institute of MIT and Harvard, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. Electronic address:
Ion channels are critical to kidney function, and their dysregulation leads to several distinct kidney diseases. Of the diversity of ion channels in kidney cells, the transient receptor potential (TRP) superfamily of proteins plays important and varied roles in both maintaining homeostasis as well as in causing disease. Recent work showed that TRPC5 blockers could successfully protect critical components of the kidney filter both in vitro and in vivo, thus revealing TRPC5 as a tractable therapeutic target for focal and segmental glomerulosclerosis (FSGS), a common cause of kidney failure.
View Article and Find Full Text PDFSmall Molecule Targets TMED9 and Promotes Lysosomal Degradation to Reverse Proteinopathy.
Cell
July 2019
Broad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address:
Intracellular accumulation of misfolded proteins causes toxic proteinopathies, diseases without targeted therapies. Mucin 1 kidney disease (MKD) results from a frameshift mutation in the MUC1 gene (MUC1-fs). Here, we show that MKD is a toxic proteinopathy.
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