Evidence map›Paper›PMID 28551800›Full record

ReviewAdvances in experimental medicine and biology2017

High-Density Lipoprotein Regulation of Mitochondrial Function.

C Roger White, Geeta Datta, Samantha Giordano

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
10.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
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  12. Inferring causal direction between two traits using RAmerican journal of human genetics · 2024
    Article
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  20. Cardiac Mitochondria Dysfunction in Dyslipidemic Mice.International journal of molecular sciences · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

C Roger WhiteDepartment of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA.
Geeta DattaDepartment of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA.
Samantha GiordanoDepartment of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA. sgiordan@uab.edu.
University of Alabama at Birmingham · US

Funding

HDL and Cellular Repair MechanismsR01DK108836 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ANANTHARAMAIAH, G M, WHITE, C ROGER · 2016 to 2019
$1.3M
Cellular Lipids and Leukocyte FunctionR01GM115367 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ANANTHARAMAIAH, G M, WHITE, C ROGER · 2015 to 2018
$1.2M
NIDDK NIH HHS R01 DK108836NIGMS NIH HHS R01 GM115367
6 · The paper itself

Abstract

Lipoproteins play a key role in regulating plasma and tissue levels of cholesterol. Apolipoprotein B (apoB)-containing lipoproteins, including chylomicrons, very-low density lipoprotein (VLDL) and low-density lipoprotein (LDL), serve as carriers of triglycerides and cholesterol and deliver these metabolites to peripheral tissues. In contrast, high-density lipoprotein (HDL) mediates Reverse Cholesterol Transport (RCT), a process by which excess cholesterol is removed from the periphery and taken up by hepatocytes where it is metabolized and excreted. Anti-atherogenic properties of HDL have been largely ascribed to apoA-I, the major protein component of the lipoprotein particle. The inflammatory response associated with atherosclerosis and ischemia-reperfusion (I-R) injury has been linked to the development of mitochondrial dysfunction. Under these conditions, an increase in reactive oxygen species (ROS) formation induces damage to mitochondrial structural elements, leading to a reduction in ATP synthesis and initiation of the apoptotic program. Recent studies suggest that HDL-associated apoA-I and lysosphingolipids attenuate mitochondrial injury by multiple mechanisms, including the suppression of ROS formation and induction of autophagy. Other apolipoproteins, however, present in lower abundance in HDL particles may exert opposing effects on mitochondrial function. This chapter examines the role of HDL-associated apolipoproteins and lipids in the regulation of mitochondrial function and bioenergetics.

Indexed as

Signal TransductionAnimalsApolipoprotein A-IAutophagyHumansLipoproteins, HDLLysophospholipidsMitochondriaMitochondrial DynamicsOxidative StressReactive Oxygen SpeciesSphingosineApolipoprotein A-ILipoproteins, HDLLysophospholipidsReactive Oxygen SpeciesSphingosinesphingosine 1-phosphateApolipoproteinsAutophagyCardiovascular diseaseCholesterolMitochondria

Identifiers

PMID28551800
PMCPMC5822681
OpenAlexW2619392341

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.