About: Mechanistic Insight of Na/K-ATPase Signaling and HO-1 into Models of Obesity and Nonalcoholic Steatohepatitis

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Mechanistic Insight of Na/K-ATPase Signaling and HO-1 into Models of Obesity and Nonalcoholic Steatohepatitis Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Mechanistic Insight of Na/K-ATPase Signaling and HO-1 into Models of Obesity and Nonalcoholic Steatohepatitis
Creator	Desauguste, Rutmann Pratt, Rebecca Sodhi, Komal Zehra, Mishghan Lakhani, Hari Pillai, Sneha
Source	PMC
abstract	Obesity is a multifaceted pathophysiological condition that has been associated with lipid accumulation, adipocyte dysfunction, impaired mitochondrial biogenesis and an altered metabolic profile. Redox imbalance and excessive release of inflammatory mediators have been intricately linked in obesity-associated phenotypes. Hence, understanding the mechanisms of redox signaling pathways and molecular targets exacerbating oxidative stress is crucial in improving health outcomes. The activation of Na/K-ATPase/Src signaling, and its downstream pathways, by reactive oxygen species (ROS) has been recently implicated in obesity and subsequent nonalcoholic steatohepatitis (NASH), which causes further production of ROS creating an oxidant amplification loop. Apart from that, numerous studies have also characterized antioxidant properties of heme oxygenase 1 (HO-1), which is suppressed in an obese state. The induction of HO-1 restores cellular redox processes, which contributes to inhibition of the toxic milieu. The novelty of these independent mechanisms presents a unique opportunity to unravel their potential as molecular targets for redox regulation in obesity and NASH. The attenuation of oxidative stress, by understanding the underlying molecular mechanisms and associated mediators, with a targeted treatment modality may provide for improved therapeutic options to combat clinical disorders.
has issue date	2019-12-21(xsd:dateTime)
bibo:doi	10.3390/ijms21010087
bibo:pmid	31877680
has license	cc-by
sha1sum (hex)	3c7d045c73a10e8b81cc58d86d7cf5d144f83b1b
schema:url	https://doi.org/10.3390/ijms21010087
resource representing a document's title	Mechanistic Insight of Na/K-ATPase Signaling and HO-1 into Models of Obesity and Nonalcoholic Steatohepatitis
has PubMed Central identifier	PMC6982200
has PubMed identifier	31877680
schema:publication	Int J Mol Sci
resource representing a document's body	covid:3c7d045c73a10e8b81cc58d86d7cf5d144f83b1b#body_text
is schema:about of	named entity 'targets' named entity 'therapeutic' named entity 'creating' named entity 'molecular' named entity 'imbalance' named entity 'numerous' named entity 'inhibition' named entity 'Mechanistic' named entity 'Signaling' named entity 'TOXIC' named entity 'THERAPEUTIC' named entity 'OXIDATIVE STRESS' named entity 'IMPROVING' named entity 'SUBSEQUENT' named entity 'CELLULAR' named entity 'UNDERLYING' named entity 'SIGNALING' named entity 'MOLECULAR' named entity 'COMBAT' named entity 'MEDIATORS' named entity 'OPTIONS' named entity 'MITOCHONDRIAL BIOGENESIS' named entity 'REACTIVE OXYGEN SPECIES' named entity 'UNIQUE' named entity 'PATHWAYS' named entity 'CLINICAL' named entity 'ALTERED' named entity 'REDOX REGULATION' named entity 'MECHANISMS' named entity 'POTENTIAL' named entity 'EXCESSIVE' named entity 'NONALCOHOLIC STEATOHEPATITIS' named entity 'OBESITY' named entity 'MULTIFACETED' named entity 'RELEASE' named entity 'PRODUCTION' named entity 'REDOX SIGNALING' named entity 'PRESENTS' named entity 'CREATING' named entity 'OXIDANT' named entity 'HO-1' named entity 'INSIGHT' named entity 'MODELS' named entity 'ATPASE' named entity 'PROCESSES' named entity 'NONALCOHOLIC STEATOHEPATITIS' named entity 'ITS' named entity 'RECENTLY' named entity 'TARGETS' named entity 'ROS' named entity 'NUMEROUS' named entity 'INDEPENDENT' named entity 'NASH' named entity 'THESE' named entity 'INHIBITION' named entity 'HAVE' named entity 'ASSOCIATED' named entity 'TARGETED' named entity 'CAUSES' named entity 'STATE' named entity 'LIPID ACCUMULATION' named entity 'OPPORTUNITY' named entity 'IMPROVED' named entity 'HEME OXYGENASE 1' named entity 'PROVIDE' named entity 'THEIR' named entity 'LOOP' named entity 'ATTENUATION' named entity 'ADIPOCYTE' named entity 'OBESITY' named entity 'METABOLIC PROFILE' named entity 'STUDIES' named entity 'IMBALANCE' named entity 'DYSFUNCTION' named entity 'UNDERSTANDING' named entity 'SUPPRESSED'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2024 OpenLink Software