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Olga A. Mareninova

Researcher at University of California, Los Angeles

Publications -  43
Citations -  2985

Olga A. Mareninova is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Pancreatitis & Acinar cell. The author has an hindex of 21, co-authored 39 publications receiving 1821 citations. Previous affiliations of Olga A. Mareninova include United States Department of Veterans Affairs & Veterans Health Administration.

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Cell death in pancreatitis: caspases protect from necrotizing pancreatitis.

Olga A. Mareninova, +7 more
- 10 Feb 2006 - 
TL;DR: The results indicate key roles for caspases, XIAP, and RIP in the regulation of cell death in pancreatitis, and suggest Manipulating these signals to change the pattern of death responses presents a therapeutic strategy for treatment of pancreatitis.
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Impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis

Olga A. Mareninova, +10 more
- 02 Nov 2009 - 
TL;DR: Autophagy is retarded in pancreatitis due to deficient lysosomal degradation caused by impaired cathepsin processing, which is associated with an imbalance between CatL and CatB, resulting in intra-acinar accumulation of active trypsin in Pancreatitis.
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Mitochondrial Dysfunction, Through Impaired Autophagy, Leads to Endoplasmic Reticulum Stress, Deregulated Lipid Metabolism, and Pancreatitis in Animal Models

György Biczó, +20 more
- 01 Feb 2018 - 
TL;DR: In different animal models, a central role is found for mitochondrial dysfunction, and for impaired autophagy as its principal downstream effector, in development of AP, a model of severe AP the pathogenesis of which has remained unknown.
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Mechanism of mitochondrial permeability transition pore induction and damage in the pancreas: inhibition prevents acute pancreatitis by protecting production of ATP

Rajarshi Mukherjee, +34 more
- 01 Aug 2016 - 
TL;DR: The mechanism and consequences of MPTP opening are demonstrated to be fundamental to multiple forms of acute pancreatitis and validates the MPTP as a drug target for this disease.