Anis Hanna

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Research Assistant Professor

Albert Einstein College of Medicine

United States

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The Role of Smad1 in Cardiac Fibrosis

Open Date: 2021-04-01

Close Date: 2023-03-31

Articles (12)

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2024

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2021

Collaborators (2)

Akihiko Kubota

Albert Einstein College of Medicine

UNITED STATES

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Nikolaos G. Frangogiannis

Albert Einstein College of Medicine

UNITED STATES

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Anis Hanna

Research Interests

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Recent Grants

Articles (12)

Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart

Cardiac Pericytes Acquire a Fibrogenic Phenotype and Contribute to Vascular Maturation After Myocardial Infarction

Diabetes Induces Cardiac Fibroblast Activation, Promoting a Matrix‐Preserving Nonmyofibroblast Phenotype, Without Stimulating Pericyte to Fibroblast Conversion

Protective effects of macrophage-specific integrin α5 in myocardial infarction are associated with accentuated angiogenesis

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

The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction

The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction

Properties and Functions of Fibroblasts and Myofibroblasts in Myocardial Infarction

Properties and Functions of Fibroblasts and Myofibroblasts in Myocardial Infarction

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

Abstract 11654: Myofibroblast Smad1 Activation Restrains Cardiac Fibrosis and Attenuates Post-Myocardial Infarction Adverse Remodeling

Abstract MP225: Macrophage-specificα5 Integrin Signaling Protects The Infarcted Heart From Adverse Remodeling By Stimulating The Angiogenic Response

Collaborators (2)

Akihiko Kubota

Nikolaos G. Frangogiannis

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