Arti V Shinde

发表

Fibroblasts in myocardial infarction: a role in inflammation and repair.

N. Frangogiannis, Nikolaos G Frangogiannis, Arti V Shinde, 2014, Journal of molecular and cellular cardiology.

Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium.

N. Frangogiannis, Bijun Chen, Anis Hanna, 2022, Journal of molecular and cellular cardiology.

Pharmacologic inhibition of the enzymatic effects of tissue transglutaminase reduces cardiac fibrosis and attenuates cardiomyocyte hypertrophy following pressure overload.

Mario J. Garcia, K. Fujikura, N. Frangogiannis, 2018, Journal of molecular and cellular cardiology.

Tissue transglutaminase induction in the pressure-overloaded myocardium regulates matrix remodelling

G. Melino, N. Frangogiannis, Ya Su, 2017, Cardiovascular research.

Thrombospondin-1 Induction in the Diabetic Myocardium Stabilizes the Cardiac Matrix in Addition to Promoting Vascular Rarefaction Through Angiopoietin-2 Upregulation

N. Frangogiannis, M. Cavalera, Carlos J. Gonzalez-Quesada, 2013, Circulation research.

Distinct roles of myofibroblast-specific Smad2 and Smad3 signaling in repair and remodeling of the infarcted heart.

N. Frangogiannis, S. Conway, Bijun Chen, 2019, Journal of molecular and cellular cardiology.

Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension.

N. Frangogiannis, Anis Hanna, Linda Alex, 2021, Matrix biology : journal of the International Society for Matrix Biology.

STIM1 Controls Endothelial Barrier Function Independently of Orai1 and Ca2+ Entry

P. Vincent, Rajender K. Motiani, M. Trebak, 2013, Science Signaling.

The group A streptococcal collagen‐like protein‐1, Scl1, mediates biofilm formation by targeting the extra domain A‐containing variant of cellular fibronectin expressed in wounded tissue

K. Martin, D. Schwegler-Berry, B. Green, 2013, Molecular microbiology.

The role of α-smooth muscle actin in fibroblast-mediated matrix contraction and remodeling.

N. Frangogiannis, Arti V Shinde, C. Humeres, 2017, Biochimica et biophysica acta. Molecular basis of disease.

Store-Independent Orai1/3 Channels Activated by Intracrine LeukotrieneC4: Role in Neointimal Hyperplasia

C. Romanin, H. Singer, Rajender K. Motiani, 2013, Circulation research.

Smad3 Signaling Promotes Fibrosis While Preserving Cardiac and Aortic Geometry in Obese Diabetic Mice

Xiao-Fan Wang, N. Frangogiannis, M. Cavalera, 2015, Circulation. Heart failure.

Mechanisms of Fibroblast Activation in the Remodeling Myocardium

N. Frangogiannis, Arti V Shinde, Arti V. Shinde, 2017, Current Pathobiology Reports.

Protective Effects of Activated Myofibroblasts in the Pressure-Overloaded Myocardium Are Mediated Through Smad-Dependent Activation of a Matrix-Preserving Program

J. Graff, N. Frangogiannis, S. Conway, 2019, Circulation research.

Tissue transglutaminase in the pathogenesis of heart failure

N. Frangogiannis, Arti V Shinde, Arti V. Shinde, 2017, Cell Death & Differentiation.

Opposing Actions of Fibroblast and Cardiomyocyte Smad3 Signaling in the Infarcted Myocardium

J. Graff, N. Frangogiannis, S. Conway, 2017, Circulation.

Identification of the Peptide Sequences within the EIIIA (EDA) Segment of Fibronectin That Mediate Integrin α9β1-dependent Cellular Activities*

R. Hynes, C. Bystroff, P. Vincent, 2008, Journal of Biological Chemistry.

Identification of the peptide sequences within the EIIIA (EDA) segment of fibronectin that mediate integrin alpha9beta1-dependent cellular activities.

R. Hynes, C. Bystroff, P. Vincent, 2008, The Journal of biological chemistry.

Aging-Associated Alterations in Myocardial Inflammation and Fibrosis: Pathophysiological Perspectives and Clinical Implications

N. Frangogiannis, Arti V Shinde, Arti V. Shinde, 2014 .

Myocardial Galectin-3 Expression Is Associated with Remodeling of the Pressure-Overloaded Heart and May Delay the Hypertrophic Response without Affecting Survival, Dysfunction, and Cardiac Fibrosis.

N. Frangogiannis, Ya Su, A. Saxena, 2016, The American journal of pathology.

The role of Interleukin Receptor Associated Kinase (IRAK)-M in regulation of myofibroblast phenotype in vitro, and in an experimental model of non-reperfused myocardial infarction.

Z. Haque, N. Frangogiannis, Ya Su, 2015, Journal of molecular and cellular cardiology.

Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of non-reperfused myocardial infarction.

N. Frangogiannis, Anis Hanna, Arti V Shinde, 2020, American journal of physiology. Heart and circulatory physiology.

Mediators secreted by myeloid cells may protect and repair the infarcted myocardium.

N. Frangogiannis, Arti V Shinde, Arti V. Shinde, 2015, Circulation research.

Myeloid-derived growth factor (C19orf10) mediates cardiac repair following myocardial infarction Mediators Secreted by Myeloid Cells May Protect and Repair the Infarcted Myocardium Commentaries on Cutting Edge Science

N. Frangogiannis, Arti V Shinde, 2015 .

Smad7 effects on TGF-β and ErbB2 restrain myofibroblast activation and protect from postinfarction heart failure

N. Frangogiannis, S. Conway, Bijun Chen, 2021, The Journal of clinical investigation.

Left atrial remodeling, hypertrophy, and fibrosis in mouse models of heart failure.

N. Frangogiannis, Ya Su, Linda Alex, 2017, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.