Search

Your search keyword '"Mulay, Shrikant R."' showing total 288 results
Start Over Author "Mulay, Shrikant R."
288 results on '"Mulay, Shrikant R."'

3. Potential of Renin-Angiotensin-Aldosterone System Modulations in Diabetic Kidney Disease: Old Players to New Hope!

Author

Malek, Vajir, Suryavanshi, Sachin V., Sharma, Nisha, Kulkarni, Yogesh A., Mulay, Shrikant R., Gaikwad, Anil Bhanudas, Pedersen, Stine Helene Falsig, Editor-in-Chief, Barber, Diane L., Series Editor, Cordat, Emmanuelle, Series Editor, Kajimura, Mayumi, Series Editor, Leipziger, Jens G., Series Editor, O'Donnell, Martha E., Series Editor, Pardo, Luis A., Series Editor, Schmitt, Nicole, Series Editor, and Stock, Christian, Series Editor

Published
2021
Full Text
View/download PDF

8. Systems biology analysis reveals role of MDM2 in diabetic nephropathy.

Author

Saito, Rintaro, Rocanin-Arjo, Anaïs, You, Young-Hyun, Darshi, Manjula, Van Espen, Benjamin, Miyamoto, Satoshi, Pham, Jessica, Pu, Minya, Romoli, Simone, Natarajan, Loki, Ju, Wenjun, Kretzler, Matthias, Nelson, Robert, Ono, Keiichiro, Thomasova, Dana, Mulay, Shrikant R, Ideker, Trey, D'Agati, Vivette, Beyret, Ergin, Belmonte, Juan Carlos Izpisua, Anders, Hans Joachim, and Sharma, Kumar

Subjects
Kidney Glomerulus, Kidney Tubules, Animals, Mice, Inbred C57BL, Mice, Knockout, Humans, Mice, Diabetic Nephropathies, Albuminuria, Diabetes Mellitus, Experimental, Computational Biology, Systems Biology, Podocytes, Proto-Oncogene Proteins c-mdm2, Inbred C57BL, Knockout, Diabetes Mellitus, Experimental
Abstract

To derive new insights in diabetic complications, we integrated publicly available human protein-protein interaction (PPI) networks with global metabolic networks using metabolomic data from patients with diabetic nephropathy. We focused on the participating proteins in the network that were computationally predicted to connect the urine metabolites. MDM2 had the highest significant number of PPI connections. As validation, significant downregulation of MDM2 gene expression was found in both glomerular and tubulointerstitial compartments of kidney biopsy tissue from 2 independent cohorts of patients with diabetic nephropathy. In diabetic mice, chemical inhibition of MDM2 with Nutlin-3a led to reduction in the number of podocytes, increased blood urea nitrogen, and increased mortality. Addition of Nutlin-3a decreased WT1+ cells in embryonic kidneys. Both podocyte- and tubule-specific MDM2-knockout mice exhibited severe glomerular and tubular dysfunction, respectively. Interestingly, the only 2 metabolites that were reduced in both podocyte and tubule-specific MDM2-knockout mice were 3-methylcrotonylglycine and uracil, both of which were also reduced in human diabetic kidney disease. Thus, our bioinformatics tool combined with multi-omics studies identified an important functional role for MDM2 in glomeruli and tubules of the diabetic nephropathic kidney and links MDM2 to a reduction in 2 key metabolite biomarkers.

Published
2016

18. Crystal Clots as Therapeutic Target in Cholesterol Crystal Embolism

Author

Shi, Chongxu, Kim, Tehyung, Steiger, Stefanie, Mulay, Shrikant R., Klinkhammer, Barbara M., Bäuerle, Tobias, Melica, Maria Elena, Romagnani, Paola, Möckel, Diana, Baues, Maike, Yang, Luying, Brouns, Sanne L.N., Heemskerk, Johan W. M., Braun, Attila, Lammers, Twan, Boor, Peter, and Anders, Hans-Joachim

Published
2020
Full Text
View/download PDF

24. Synchronized renal tubular cell death involves ferroptosis

Author

Linkermann, Andreas, Skouta, Rachid, Himmerkus, Nina, Mulay, Shrikant R., Dewitz, Christin, De Zen, Federica, Prokai, Agnes, Zuchtriegel, Gabriele, Krombach, Fritz, Welz, Patrick-Simon, Weinlich, Ricardo, Berghe, Tom Vanden, Vandenabeele, Peter, Pasparakis, Manolis, Bleich, Markus, Weinberg, Joel M., Reichel, Christoph A., Bräsen, Jan Hinrich, Kunzendorf, Ulrich, Anders, Hans-Joachim, Stockwell, Brent R., Green, Douglas R., Krautwald, Stefan, and Dixit, Vishva M.

Published
2014

34. Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1β secretion

Author

Mulay, Shrikant R., Kulkarni, Onkar P., Rupanagudi, Khader V., Migliorini, Adriana, Darisipudi, Murthy N., Vilaysane, Akosua, Muruve, Daniel, Shi, Yan, Munro, Fay, Liapis, Helen, and Anders, Hans-Joachim

Subjects
Research, Health aspects, Calcium (Nutrient) -- Health aspects, Inflammation -- Research, Kidney stones -- Research, Oxalates -- Health aspects, Calcium, Dietary -- Health aspects
Abstract

Nephrocalcinosis, acute calcium oxalate (CaOx) nephropathy, and renal stone disease can lead to inflammation and subsequent renal failure, but the underlying pathological mechanisms remain elusive. Other crystallopathies, such as gout, [...]

Published
2013
Full Text
View/download PDF

38. Inhibitors of Calcium Oxalate Crystallization for the Treatment of Oxalate Nephropathies

Author

Kletzmayr, Anna, Mulay, Shrikant R., Motrapu, Manga, Luo, Zhi, Anders, Hans-Joachim, Ivarsson, Mattias E., and Leroux, Jean-Christophe

Subjects
image‐based drug screening, kidney stones, kidney calcification, lcsh:Q, image-based drug screening, lcsh:Science, calcium oxalate crystallization inhibitors, chronic kidney disease
Abstract

Calcium oxalate (CaOx) crystal‐induced nephropathies comprise a range of kidney disorders, for which there are no efficient pharmacological treatments. Although CaOx crystallization inhibitors have been suggested as a therapeutic modality already decades ago, limited progress has been made in the discovery of potent molecules with efficacy in animal disease models. Herein, an image‐based machine learning approach to systematically screen chemically modified myo‐inositol hexakisphosphate (IP6) analogues is utilized, which enables the identification of a highly active divalent inositol phosphate molecule. To date, this is the first molecule shown to completely inhibit the crystallization process in the nanomolar range, reduce crystal–cell interactions, thereby preventing CaOx‐induced transcriptomic changes, and decrease renal CaOx deposition and kidney injury in a mouse model of hyperoxaluria. In conclusion, IP6 analogues based on such a scaffold may represent a new treatment option for CaOx nephropathies., Advanced Science, 7 (8), ISSN:2198-3844

Published
2020

41. Endoplasmic Reticulum Stress and Renin-Angiotensin System Crosstalk in Endothelial Dysfunction

Author

Mulay, Shrikant R., Gaikwad, Anil Bhanudas, Sankrityayan, Himanshu, Rao, Pooja Dhileepkumar, Shelke, Vishwadeep, and Kulkarni, Yogesh A.

Abstract

Background: Vascular endothelial dysfunction (VED) significantly results in catastrophic cardiovascular diseases with multiple aetiologies. Variations in vasoactive peptides, including angiotensin II and endothelin 1, and metabolic perturbations like hyperglycaemia, altered insulin signalling, and homocysteine levels result in pathogenic signalling cascades, which ultimately lead to VED. Endoplasmic reticulum (ER) stress reduces nitric oxide availability, causes aberrant angiogenesis, and enhances oxidative stress pathways, consequently promoting endothelial dysfunction. Moreover, the renin-angiotensin system (RAS) has widely been acknowledged to impact angiogenesis, endothelial repair and inflammation. Interestingly, experimental studies at the preclinical level indicate a possible pathological link between the two pathways in the development of VED. Furthermore, pharmacological modulation of ER stress ameliorates angiotensin-II mediated VED as well as RAS intervention either through inhibition of the pressor arm or enhancement of the depressor arm of RAS, mitigating ER stress-induced endothelial dysfunction and thus emphasizing a vital crosstalk. Conclusion: Deciphering the pathway overlap between RAS and ER stress may open potential therapeutic avenues to combat endothelial dysfunction and associated diseases. Several studies suggest that alteration in a component of RAS may induce ER stress or induction of ER stress may modulate the RAS components. In this review, we intend to elaborate on the crosstalk of ER stress and RAS in the pathophysiology of VED.

Published
2023
Full Text
View/download PDF

47. Cellular and Molecular Mechanisms of Kidney Injury in 2,8-Dihydroxyadenine Nephropathy

Author

Klinkhammer, Barbara Mara, primary, Djudjaj, Sonja, additional, Kunter, Uta, additional, Palsson, Runolfur, additional, Edvardsson, Vidar Orn, additional, Wiech, Thorsten, additional, Thorsteinsdottir, Margret, additional, Hardarson, Sverrir, additional, Foresto-Neto, Orestes, additional, Mulay, Shrikant R., additional, Moeller, Marcus Johannes, additional, Jahnen-Dechent, Wilhelm, additional, Floege, Jürgen, additional, Anders, Hans-Joachim, additional, and Boor, Peter, additional

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results