Matthew D. Plotkin
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Also affiliated: Brigham and Women's Hospital (1996–2001); Boston Children's Hospital (1996); Mayo Clinic (1993); Harvard University (1996–2001); New York Medical College (2006–2014); University of Arkansas Medical Center (2018–2020); University of Missouri Hospital (2020); University of Missouri Health System (2020); Central Arkansas Veterans Healthcare System (2020); Renal Research Institute (2006–2010); John L. McClellan Memorial Veterans Hospital (2018–2020)
Research Areas
Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Matthew D. Plotkin's research has focused on the expression and function of ion cotransporters, particularly the Na-K-2Cl cotransporter (BSC) and the thiazide-sensitive Na-Cl cotransporter (TSC) in the kidney and nervous system. His early work investigated the developmental regulation of these transporters in rat brains and their potential role in GABA's excitatory function in immature brains. Publications also detail the localization of rTSC1 in the rat kidney and the apical localization of rBSC1 on rat thick ascending limbs. More recently, his work has explored the contribution of kidney-derived mesenchymal stem cells to vasculogenesis, angiogenesis, and endothelial repair. Studies have shown that microparticles from these cells carry proangiogenic signals and aid recovery from acute kidney injury. His research also encompasses the differentiation of mesenchymal cells from adult kidneys into various interstitial cell types, including erythropoietin-producing fibroblasts, and their support of angiogenesis.
Metrics
- h-index: 17
- Publications: 26
- Citations: 2,017
Selected Publications
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Genome-Wide DNA Methylation Signatures Predict the Early Asymptomatic Doxorubicin-Induced Cardiotoxicity in Breast Cancer (2021)
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A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress (2020)
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Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice (2020)
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Id1 expression in kidney endothelial cells protects against diabetes‐induced microvascular injury (2020)
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Young blood for old kidneys? More questions than answers so far (2018)
Collaboration Network
Top Collaborators
- Id1 expression in kidney endothelial cells protects against diabetes‐induced microvascular injury
- A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress
- Genome-Wide DNA Methylation Signatures Predict the Early Asymptomatic Doxorubicin-Induced Cardiotoxicity in Breast Cancer
- A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress
- Genome-Wide DNA Methylation Signatures Predict the Early Asymptomatic Doxorubicin-Induced Cardiotoxicity in Breast Cancer
- A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- Depletion of senescent-like neuronal cells alleviates cisplatin-induced peripheral neuropathy in mice
- A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress
- A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress
- A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress
- Genome-Wide DNA Methylation Signatures Predict the Early Asymptomatic Doxorubicin-Induced Cardiotoxicity in Breast Cancer
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