Monowar Aziz

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Associate Professor

Feinstein Institute for Medical Research

United States

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About

Monowar Aziz is an Associate Professor at the Feinstein Institute for Medical Research in the United States. His research primarily focuses on the roles of extracellular proteins and microRNAs in inflammation, sepsis, and tissue injury as evidenced by his recent publications. He has investigated various mechanisms impacting neutrophil functions and their implications in conditions such as hepatic ischemia and cancer-related inflammation.

Recent Grants

Grant: Close

Neutrophils in Sepsis: Role of CIRP

Open Date: 2018-07-01

Close Date: 2023-06-01

Grant: Close

Neutrophils in Sepsis: Role of CIRP

Open Date: 2018-06-01

Close Date: 2020-06-01

Articles (15)

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2025

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2020

Collaborators (10)

Mikala Egeblad

Johns Hopkins University

UNITED STATES

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Ilaria Malanchi

The Francis Crick Institute

UNITED KINGDOM

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Betsy Barnes

Professor

Hofstra University North Shore Long Island Jewish School of Medicine

UNITED STATES

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Kensuke Murata

Juntendo University

JAPAN

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Andrés Hidalgo

Yale University

UNITED STATES

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Yuichi Akama

Feinstein Institute for Medical Research

UNITED STATES

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Borko Amulic

University of Bristol

UNITED KINGDOM

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Ping Wang

Professor, Chief Scientific Officer

Feinstein Institute for Medical Research

UNITED STATES

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Max Brenner

Associate Professor

Elmezzi Graduate School of Molecular Medicine

UNITED STATES

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Etienne Meylan

Associate Professor

Université libre de Bruxelles

BELGIUM

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Monowar Aziz

Research Interests

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About

Recent Grants

Articles (15)

Extracellular Cold-Inducible RNA-Binding Protein: Progress from Discovery to Present

Milk fat globule-epidermal growth factor-VIII–derived oligopeptide 3 (MOP3) attenuates inflammation and improves survival in hepatic ischemia/reperfusion injury

Neutrophils disrupt B-1a cell homeostasis by targeting Siglec-G to exacerbate sepsis

Extracellular CIRP induces CD4CD8αα intraepithelial lymphocyte cytotoxicity in sepsis

Harnessing Extracellular microRNAs for Diagnostics and Therapeutics in Acute Systemic Inflammation

A Synthetic Poly(A) Tail Targeting Extracellular CIRP Inhibits Sepsis

Antigen-presenting aged neutrophils induce CD4+ T cells to exacerbate inflammation in sepsis

Extracellular CIRP Induces Novel Nectin-2+ (CD112+) Neutrophils to Promote Th1 Differentiation in Sepsis

Neutrophil phenotypes and functions in cancer: A consensus statement

Active Release of eCIRP via Gasdermin D Channels to Induce Inflammation in Sepsis

Extracellular CIRP decreases Siglec-G expression on B-1a cells skewing them towards a pro-inflammatory phenotype in sepsis

Inhibition of Efferocytosis by Extracellular CIRP–Induced Neutrophil Extracellular Traps

Frontline Science: Extracellular CIRP generates a proinflammatory Ly6G+CD11bhi subset of low-density neutrophils in sepsis

Therapeutic Potential of B-1a Cells in COVID-19.

Frontline Science: Extracellular CIRP generates a proinflammatory Ly6G+ CD11bhi subset of low-density neutrophils in sepsis.

Collaborators (10)

Mikala Egeblad

Ilaria Malanchi

Betsy Barnes

Kensuke Murata

Andrés Hidalgo

Yuichi Akama

Borko Amulic

Ping Wang

Max Brenner

Etienne Meylan

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