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Matthew J. Justice

Researcher at Indiana University

Publications -  6
Citations -  5531

Matthew J. Justice is an academic researcher from Indiana University. The author has contributed to research in topics: Autophagy & Ceramide. The author has an hindex of 5, co-authored 6 publications receiving 5060 citations. Previous affiliations of Matthew J. Justice include Indiana University – Purdue University Indianapolis & University of Colorado Denver.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

17β-Estradiol Attenuates Hypoxic Pulmonary Hypertension via Estrogen Receptor–mediated Effects

TL;DR: E2 attenuates hemodynamic and remodeling parameters in HPH in an ER-dependent manner, through direct antiproliferative mechanisms on vascular cells, which may provide novel nonhormonal therapeutic targets for HPH.
Journal ArticleDOI

Mechanisms of lung endothelial barrier disruption induced by cigarette smoke: role of oxidative stress and ceramides

TL;DR: In this article, the authors investigated the occurrence and mechanisms by which soluble components of mainstream CS disrupt the lung endothelial cell barrier function using cultured primary rat microvascular cell monolayers.
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Sphingolipid regulation of lung epithelial cell mitophagy and necroptosis during cigarette smoke exposure

TL;DR: DHCs, in particular, C24‐DHC, are implicate as protective against CS toxicity by enhancing autophagy, whereas C16‐Cer accumulation contributes to mitochondrial damage and PINKl‐mediated necroptosis, which may be amplified by the inhibition of C24-DHC‐producing CerS2.
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Alpha-1 antitrypsin supplementation improves alveolar macrophages efferocytosis and phagocytosis following cigarette smoke exposure.

TL;DR: A1AT significantly improved AM global engulfment, including phagocytosis, even when cells were simultaneously challenged with apoptotic and Fc-coated (bacteria-like) targets, and may render A1AT as a potential therapy for COPD exacerbations.