Oxysterol-binding protein-like 7 deficiency leads to ER stress-mediated apoptosis in podocytes and proteinuria

Author:

Duara Joanne12ORCID,Torres Maria13,Gurumani Margaret13,Molina David Judith14,Njeim Rachel14ORCID,Kim Jin-Ju14,Mitrofanova Alla14ORCID,Ge Mengyuan14,Sloan Alexis14,Müller-Deile Janina5ORCID,Schiffer Mario56ORCID,Merscher Sandra14ORCID,Fornoni Alessia14ORCID

Affiliation:

1. Peggy and Harold Katz Family Drug Discovery Center, University of Miami Miller School of Medicine, Miami, Florida, United States

2. Department of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute, Holtz Children’s Hospital, University of Miami Miller School of Medicine, Miami, Florida, United States

3. Boston University, Boston, Massachusetts, United States

4. Katz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, United States

5. Department of Nephrology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany

6. Mount Desert Island Biological Laboratories, Salisbury Cove, Maine, United States

Abstract

OSBPL7 and ER stress comprise a central mechanism in glomerular injury. This study highlights a crucial link between OSBPL7 deficiency and ER stress in CKD. OSBPL7 deficiency causes ER stress, leading to podocyte apoptosis. There is a selective effect on lipid homeostasis in that OSBPL7 deficiency affects lipid homeostasis, altering cellular triglyceride but not cholesterol content. The interaction of ER stress and apoptosis supports that ER stress, not reduced autophagy, is the main driver of apoptosis in OSBPL7-deficient podocytes.

Funder

NIH National Institutes of Health

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

American Physiological Society

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