Maja T. Lindenmeyer

ORCID: 0000-0003-4162-9107
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About
Contact & Profiles
Research Areas
  • Renal Diseases and Glomerulopathies
  • Chronic Kidney Disease and Diabetes
  • Renal and related cancers
  • T-cell and B-cell Immunology
  • Genetic and Kidney Cyst Diseases
  • Single-cell and spatial transcriptomics
  • Sesquiterpenes and Asteraceae Studies
  • COVID-19 Clinical Research Studies
  • Immune Cell Function and Interaction
  • Plant Toxicity and Pharmacological Properties
  • Systemic Sclerosis and Related Diseases
  • Cellular Mechanics and Interactions
  • Pancreatic function and diabetes
  • Systemic Lupus Erythematosus Research
  • Macrophage Migration Inhibitory Factor
  • Cancer-related molecular mechanisms research
  • Cell Adhesion Molecules Research
  • Erythrocyte Function and Pathophysiology
  • Cancer Genomics and Diagnostics
  • Vasculitis and related conditions
  • Nuclear Receptors and Signaling
  • Reproductive System and Pregnancy
  • Immunotherapy and Immune Responses
  • GDF15 and Related Biomarkers
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema

University Medical Center Hamburg-Eppendorf
2018-2025

Universität Hamburg
2018-2025

Ludwig-Maximilians-Universität München
2007-2022

Swiss Integrative Center for Human Health
2008-2020

University of Zurich
2008-2020

LMU Klinikum
2008-2019

München Klinik
2019

Institut für Urheber- und Medienrecht
2018

Polyclinic Medical Center
2018

University Hospital of Zurich
2008-2016

Injury and loss of podocytes are leading factors glomerular disease renal failure. The postmitotic podocyte is the primary target for toxic, immune, metabolic, oxidant stress, but little known about how this cell type copes with stress. Recently, autophagy has been identified as a major pathway that delivers damaged proteins organelles to lysosomes in order maintain cellular homeostasis. Here we report exhibit an unusually high level constitutive autophagy. Podocyte-specific deletion...

10.1172/jci39492 article EN Journal of Clinical Investigation 2010-03-08

Diabetic kidney disease is the leading cause of ESRD, but few biomarkers diabetic are available. This study used gas chromatography-mass spectrometry to quantify 94 urine metabolites in screening and validation cohorts patients with diabetes mellitus (DM) CKD(DM+CKD), DM without CKD (DM–CKD), healthy controls. Compared levels controls, 13 were significantly reduced DM+CKD (P≤0.001), 12 remained significant when compared DM–CKD cohort. Many differentially expressed water-soluble organic...

10.1681/asn.2013020126 article EN Journal of the American Society of Nephrology 2013-08-16

Chronic glomerular diseases, associated with renal failure and cardiovascular morbidity, represent a major health issue. However, they remain poorly understood. Here we have reported that tightly controlled mTOR activity was crucial to maintaining podocyte function, while dysregulation of facilitated diseases. Genetic deletion complex 1 (mTORC1) in mouse podocytes induced proteinuria progressive glomerulosclerosis. Furthermore, simultaneous both mTORC1 mTORC2 from aggravated the lesions,...

10.1172/jci44774 article EN Journal of Clinical Investigation 2011-05-23

Extrapulmonary manifestations of COVID-19 have gained attention due to their links clinical outcomes and potential long-term sequelae1. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) displays tropism towards several organs, including the heart kidney. Whether it also directly affects liver has been debated2,3. Here we provide clinical, histopathological, molecular bioinformatic evidence for hepatic SARS-CoV-2. We find that injury, indicated by a high frequency abnormal function...

10.1038/s42255-022-00552-6 article EN cc-by Nature Metabolism 2022-03-28

The endoplasmic reticulum (ER) is an important site for protein folding and becomes "stressed" when its capacity to fold proteins overwhelmed. In response, "unfolded response" (UPR) genes are induced, increasing the proteins; if response insufficient, then apoptosis ensues. For investigation of whether proteinuria hyperglycemia induce ER stress in renal epithelial cells, microarray data from biopsies established diabetic nephropathy (DN) were analyzed. Expression UPR was significantly...

10.1681/asn.2007121313 article EN Journal of the American Society of Nephrology 2008-09-06

Diabetic nephropathy (DN) is a frequent complication in patients with diabetes. Although the majority of DN models and human studies have focused on glomeruli, tubulointerstitial damage major feature an important predictor renal dysfunction. This study sought to investigate molecular markers pathogenic pathways interstitium DN. Microdissected compartments from biopsies established control kidneys were subjected expression profiling. Analysis candidate genes, potentially involved basis common...

10.1681/asn.2006121304 article EN Journal of the American Society of Nephrology 2007-05-03

Lupus nephritis (LN) is a serious manifestation of systemic lupus erythematosus. Therapeutic studies in mouse LN models do not always predict outcomes human therapeutic trials, raising concerns about the relevance these preclinical models. In this study, we used an unbiased transcriptional network approach to define, molecular terms, similarities and differences among three LN. Genome-wide gene-expression networks were generated using natural language processing automated promoter analysis...

10.4049/jimmunol.1103031 article EN The Journal of Immunology 2012-06-21

Apoptosis of podocytes is considered critical in the pathogenesis diabetic nephropathy (DN). Free fatty acids (FFAs) are critically involved diabetes mellitus type 2, particular regulation pancreatic β cell survival. The objectives this study were to elucidate role palmitic acid, palmitoleic, and oleic acid podocyte death endoplasmic reticulum (ER) stress. We show that increases death, both apoptosis necrosis podocytes, a dose time-dependent fashion. Palmitic induces ER stress, leading an...

10.1152/ajprenal.00196.2010 article EN AJP Renal Physiology 2010-07-29

<h3>Objectives</h3> To characterise renal tissue metabolic pathway gene expression in different forms of glomerulonephritis. <h3>Methods</h3> Patients with nephrotic syndrome (NS), antineutrophil cytoplasmic antibody-associated vasculitis (AAV), systemic lupus erythematosus (SLE) and healthy living donors (LD) were studied. Clinically indicated biopsies obtained at time diagnosis microdissected into glomerular tubulointerstitial compartments. Microarray-derived differential 88 genes...

10.1136/annrheumdis-2017-212935 article EN Annals of the Rheumatic Diseases 2018-05-03

Although it is well established that microbial infections predispose to autoimmune diseases, the underlying mechanisms remain poorly understood. After infection, tissue-resident memory T (TRM) cells persist in peripheral organs and provide immune protection against reinfection. However, whether TRM participate responses unrelated primary such as inflammation, unknown. By using high-dimensional single-cell analysis, we identified CD4+ with a TH17 signature (termed TRM17 cells) kidneys of...

10.1126/sciimmunol.aba4163 article EN Science Immunology 2020-08-07

The cellular origins of glomerulosclerosis involve activation parietal epithelial cells (PECs) and progressive podocyte depletion. While mammalian target rapamycin-mediated (mTOR-mediated) hypertrophy is recognized as an important signaling pathway in the context glomerular disease, role a compensatory mechanism preventing PEC remains poorly understood. In this study, we show that mTOR activation-related genes were both upregulated intercorrelated biopsies from patients with focal segmental...

10.1172/jci.insight.99271 article EN JCI Insight 2019-09-18

Significance Statement The ability to produce glucose from nonhexose precursors is a main metabolic function of renal proximal tubule (PT) cells. PT cells adapt metabolically during CKD, but little known about gluconeogenesis in chronically injured Our study demonstrates the progressive loss enzymes animal models and CKD patients parallel global change pathway expression activation injury pathways. This alteration not only due has systemic repercussions on lactate levels experimental human...

10.1681/asn.2021050680 article EN Journal of the American Society of Nephrology 2022-03-10

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and histopathologic glomerular lesions are among earliest structural alterations DN. However, signaling pathways that initiate these incompletely understood.To delineate cellular molecular basis for DN initiation, we performed single-cell bulk RNA sequencing cells from type 2 diabetes mice (BTBR ob/ob) at early stage DN.Analysis differentially expressed genes revealed glucose-independent responses in cell types. The...

10.1186/s13073-022-01145-4 article EN cc-by Genome Medicine 2023-01-10

Kidney diseases impart a vast burden on affected individuals and the overall health care system. Progressive loss of renal parenchymal cells functional decline following injury are often observed. Notch-1 -2 receptors crucially involved in nephron development contribute to inflammatory kidney diseases. We specifically determined participation receptor Notch-3 tubulointerstitial responses. Here we show by heat map analyses that transcripts up-regulated human A similar response was...

10.1002/path.4076 article EN The Journal of Pathology 2012-07-19

Endothelial dysfunction is a central pathomechanism in diabetes-associated complications. We hypothesized pathogenic role this of cathepsin S (Cat-S), cysteine protease that degrades elastic fibers and activates the protease-activated receptor-2 (PAR2) on endothelial cells. found injection mice with recombinant Cat-S induced albuminuria glomerular cell injury PAR2-dependent manner. In vivo microscopy confirmed for intrinsic Cat-S/PAR2 ischemia-induced microvascular permeability. vitro...

10.1681/asn.2015020208 article EN Journal of the American Society of Nephrology 2015-11-13
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