M. Nieman

发表

Ablation of the calpain-targeted site in cardiac myosin binding protein-C is cardioprotective during ischemia-reperfusion injury.

Erik N. Taylor, D. Kass, R. Gilbert, 2019, Journal of molecular and cellular cardiology.

Impaired Cardiac Contractility in Mice Lacking Both the AE3 \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{Cl}^{-}{/}\mathrm{HCO}_{3}^{-}\) \end{document} Exchanger and the NKCC1 N

T. Doetschman, M. Ashraf, Yigang Wang, 2008, Journal of Biological Chemistry.

Decreased blood pressure and vascular smooth muscle tone in mice lacking basolateral Na(+)-K(+)-2Cl(-) cotransporter.

J. Lorenz, G. Shull, R. Paul, 2002, American journal of physiology. Heart and circulatory physiology.

Accelerated onset of heart failure in mice during pressure overload with chronically decreased SERCA2 calcium pump activity.

J. Lorenz, G. Shull, T. Kimball, 2004, American journal of physiology. Heart and circulatory physiology.

Altered dose response to beta-agonists in SERCA1a-expressing hearts ex vivo and in vivo.

S. Huke, I. Grupp, J. Lorenz, 2002, American journal of physiology. Heart and circulatory physiology.

Impaired Cardiac Performance in Heterozygous Mice with a Null Mutation in the Sarco(endo)plasmic Reticulum Ca2+-ATPase Isoform 2 (SERCA2) Gene*

T. Doetschman, J. Lorenz, G. Shull, 1999, The Journal of Biological Chemistry.

Pharmacologic Inhibition of Pain Response to Incomplete Vascular Occlusion Blunts Cardiovascular Preconditioning Response.

Nathan Robbins, Jack Rubinstein, J. Lorenz, 2021, Cardiovascular toxicology.

Renal salt wasting in mice lacking NHE3 Na+/H+ exchanger but not in mice lacking NHE2.

J. Lorenz, G. Shull, P. Schultheis, 2001, American journal of physiology. Renal physiology.

hypertension using a modified two-kidney , one-clip approach in mice is not dependent on the 1 or 2 NaK-ATPase ouabain-binding site

J. Lingrel, J. Lorenz, V. Prasad, 2011 .

Renovascular hypertension using a modified two-kidney, one-clip approach in mice is not dependent on the α1 or α2 Na-K-ATPase ouabain-binding site.

J. Lingrel, J. Lorenz, V. Prasad, 2011, American journal of physiology. Renal physiology.

The non-diuretic hypotensive effects of thiazides are enhanced during volume depletion states

Jack Rubinstein, J. Lorenz, Min Jiang, 2017, PloS one.

Inhibition of Senescence‐Associated Genes Rb1 and Meis2 in Adult Cardiomyocytes Results in Cell Cycle Reentry and Cardiac Repair Post–Myocardial Infarction

Yigang Wang, A. Paul, S. Sadayappan, 2019, Journal of the American Heart Association.

Pharmacological and Activated Fibroblast Targeting of Gβγ-GRK2 After Myocardial Ischemia Attenuates Heart Failure Progression.

J. Molkentin, J. Lorenz, Íñigo Valiente-Alandí, 2017, Journal of the American College of Cardiology.

Fibroblast growth factor-2 mediates pressure-induced hypertrophic response.

S. Pawlowski, T. Doetschman, J. Lorenz, 1999, The Journal of clinical investigation.

Expression of R120G–αB-Crystallin Causes Aberrant Desmin and αB-Crystallin Aggregation and Cardiomyopathy in Mice

T. Hewett, J. Lorenz, A. Gerdes, 2001 .

Expression of R120G-alphaB-crystallin causes aberrant desmin and alphaB-crystallin aggregation and cardiomyopathy in mice.

T. Hewett, J. Lorenz, A. Gerdes, 2001, Circulation research.

Transient receptor potential vanilloid 2 function regulates cardiac hypertrophy via stretch-induced activation

Sheryl E. Koch, Nathan Robbins, Jack Rubinstein, 2017, Journal of hypertension.

Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction.

J. Lingrel, J. Lorenz, M. Nieman, 2013, American journal of physiology. Heart and circulatory physiology.

Tranilast Blunts the Hypertrophic and Fibrotic Response to Increased Afterload Independent of Cardiomyocyte Transient Receptor Potential Vanilloid 2 Channels

Sheryl E. Koch, Nathan Robbins, Jack Rubinstein, 2018, Journal of cardiovascular pharmacology.

Increased sensitivity to K+ deprivation in colonic H,K-ATPase-deficient mice.

T. Doetschman, P. Meneton, J. Lorenz, 1998, The Journal of clinical investigation.

Mouse Model of Desmin-Related Cardiomyopathy

G. Dorn, J. Lorenz, A. Gerdes, 2001, Circulation.

Phenotype Resembling Gitelman’s Syndrome in Mice Lacking the Apical Na+-Cl− Cotransporter of the Distal Convoluted Tubule*

T. Doetschman, P. Meneton, J. Lorenz, 1998, The Journal of Biological Chemistry.

Single-cell transcriptomic profiling of kidney fibrosis identifies a novel specific fibroblast marker and putative disease target

D. Lindquist, M. Adam, P. Devarajan, 2022, bioRxiv.

Knockout of the Na,K-ATPase α₂-isoform in the cardiovascular system does not alter basal blood pressure but prevents ACTH-induced hypertension.

J. Lingrel, J. Lorenz, J. Neumann, 2011, American journal of physiology. Heart and circulatory physiology.

SERCA2 Haploinsufficiency in a Mouse Model of Darier Disease Causes a Selective Predisposition to Heart Failure

Wei Huang, Yigang Wang, J. Lorenz, 2015, BioMed research international.

Ablation of plasma membrane Ca(2+)-ATPase isoform 4 prevents development of hypertrophy in a model of hypertrophic cardiomyopathy.

Jack Rubinstein, J. Lorenz, V. Prasad, 2014, Journal of molecular and cellular cardiology.

Blood pressure maintenance in NHE3-deficient mice with transgenic expression of NHE3 in small intestine.

J. Lorenz, V. Prasad, G. Shull, 2005, American journal of physiology. Regulatory, integrative and comparative physiology.

CLIC5 mutant mice are resistant to diet-induced obesity and exhibit gastric hemorrhaging and increased susceptibility to torpor.

Vikram Prasad, P. Tso, J. Lorenz, 2010, American journal of physiology. Regulatory, integrative and comparative physiology.

Interaction between transcellular and paracellular water transport pathways through Aquaporin 5 and the tight junction complex

G. Boivin, J. Lorenz, A. Hand, 2007, Proceedings of the National Academy of Sciences.

TGF-beta1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II.

T. Doetschman, T. Kimball, S. Witt, 2002, The Journal of clinical investigation.

TGF-β1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II

T. Doetschman, T. Kimball, S. Witt, 2002 .

Inhibiting Fibronectin Attenuates Fibrosis and Improves Cardiac Function in a Model of Heart Failure

J. Molkentin, J. Lorenz, S. Potter, 2018, Circulation.

Loss of the AE3 Cl−/HCO−3 exchanger in mice affects rate-dependent inotropy and stress-related AKT signaling in heart

J. Lorenz, V. Prasad, G. Shull, 2013, Front. Physiol..

Adipocyte deletion of the RNA binding protein HuR induces cardiac hypertrophy and fibrosis

J. Benoit, P. Alam, M. Nieman, 2021, bioRxiv.

Consumption of high fat diet acutely prior to ischemia / reperfusion results in 1 cardioprotection through NF-κB dependent regulation of autophagic pathways

Sheryl E. Koch, Jack Rubinstein, S. Koch, 2014 .

Adipocyte deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis.

J. Benoit, A. P. Owens, P. Alam, 2021, American journal of physiology. Heart and circulatory physiology.

HuR inhibition reduces post-ischemic cardiac remodeling by dampening acute inflammatory gene expression and the innate immune response

J. Aubé, A. P. Owens, P. Alam, 2023, bioRxiv.

Uroguanylin knockout mice have increased blood pressure and impaired natriuretic response to enteral NaCl load.

J. Lorenz, L. Gawenis, Mitchell Cohen, 2003, The Journal of clinical investigation.

Human antigen R as a therapeutic target in pathological cardiac hypertrophy.

Nathan Robbins, Jack Rubinstein, J. Lorenz, 2019, JCI insight.

Loss of NHE1 activity leads to reduced oxidative stress in heart and mitigates high-fat diet-induced myocardial stress.

Yigang Wang, J. Lorenz, V. Prasad, 2013, Journal of molecular and cellular cardiology.

Single-cell sequencing dissects the transcriptional identity of activated fibroblasts and identifies novel persistent distal tubular injury patterns in kidney fibrosis

D. Lindquist, P. Devarajan, Andrew S. Potter, 2023, Research square.

Amino terminus of cardiac myosin binding protein-C regulates cardiac contractility.

M. Zilliox, T. Irving, R. Gilbert, 2021, Journal of molecular and cellular cardiology.

Overexpression of miR-223 Tips the Balance of Pro- and Anti-hypertrophic Signaling Cascades toward Physiologic Cardiac Hypertrophy*

Xiaohong Wang, Yutian Li, Wei Huang, 2016, The Journal of Biological Chemistry.

Acute consumption of a high-fat diet prior to ischemia-reperfusion results in cardioprotection through NF-κB-dependent regulation of autophagic pathways.

Sheryl E. Koch, Jack Rubinstein, S. Koch, 2014, American journal of physiology. Heart and circulatory physiology.

Human antigen R as a therapeutic target in pathological cardiac hypertrophy.

Nathan Robbins, Jack Rubinstein, Liang Xu, 2019, JCI insight.

Loss of NHE1 activity leads to reduced oxidative stress in heart and mitigates high-fat diet-induced myocardial stress.

Yigang Wang, J. Lorenz, V. Prasad, 2013, Journal of molecular and cellular cardiology.