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Am J Transl Res 2021 15;13(3):1233-1244. Epub 2021 Mar 15.

Department of Nephrology, Guang Xing Hospital Affiliated to Zhejiang Chinese Medical University Hangzhou, China.

The epithelial-mesenchymal transition (EMT) is usually considered the central mechanism of podocyte injury that eventually leads to proteinuria. We used an TGF-β1 induced podocyte EMT model and an rat focal segmental glomerulosclerosis (FSGS) model to uncover the mechanism underlying the protective effect of triptolide (TP) on podocytes. We found that TP could reverse the podocyte EMT process and upregulate the expression of TET2 in the TGF-β1-induced podocyte injury model. Read More

J Physiol Biochem 2021 Apr 9. Epub 2021 Apr 9.

Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad, India.

Hypoxia-inducible factor1 (HIF1) plays a pivotal role in ensuring cells adapt to low-oxygen conditions. Depletion of oxygen, a co-substrate during hydroxylation of prolyl (P402 and P564) residues of HIF1⍺, evades HIF1⍺ ubiquitination and enables its dimerization with HIF1β to mediate global transcriptional response to hypoxia. Though HIF1 is largely considered eliciting a protective role during physiological or pathological hypoxia or ischemia, elevated HIF1 during chronic hypoxia contributes to glomerular diseases' pathology and proteinuria. Read More

J Am Soc Nephrol 2021 Apr 1. Epub 2021 Apr 1.

Division of Nephrology and Hypertension, Department of Medicine, UNC Kidney Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

Background: Podocyte slit diaphragms (SDs) are intercellular junctions that function as size-selective filters, excluding most proteins from urine. Abnormalities in SDs cause proteinuria and nephrotic syndrome. Podocytes exhibit apicobasal polarity, which can affect fundamental aspects of cell biology, including morphology, intercellular junction formation, and asymmetric protein distribution along the plasma membrane. Read More

Pediatr Nephrol 2021 Mar 31. Epub 2021 Mar 31.

Institut Imagine, Laboratoire des maladies rénales héréditaires, INSERM UMR 1163, Université de Paris, Paris, France.

Genetic studies of hereditary nephrotic syndrome (NS) have identified more than 50 genes that, if mutated, are responsible for monogenic forms of steroid-resistant NS (SRNS), either isolated or syndromic. Most of these genes encode proteins expressed in the podocyte with various functions such as transcription factors, mitochondrial proteins, or enzymes, but mainly structural proteins of the slit diaphragm (SD) as well as cytoskeletal binding and regulator proteins. Syndromic NS is sometimes associated with neurological features. Read More

JCI Insight 2021 Mar 30. Epub 2021 Mar 30.

Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, United States of America.

Lupus nephritis (LN) is a serious complication occurring in 50% of patients with systemic lupus erythematosus (SLE) for which there is lack of biomarkers, specific medications, and a clear understanding of its pathogenesis. The expression of calcium/calmodulin kinase IV (CaMK4) is increased in podocytes of patients with LN and lupus-prone mice and its podocyte-targeted inhibition averts the development of nephritis in mice. Nephrin is a key podocyte molecule essential for the maintenance of the glomerular slit diaphragm. Read More