Evidence map›Paper›PMID 21976778›Full record

ReviewJournal of lipid research2011

Early steps in steroidogenesis: intracellular cholesterol trafficking.

Walter L Miller, Himangshu S Bose

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers.

0numbers the graph read from it
0cells of the map it votes in
243citing papers in PubMed
28.0field-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

243 citing papers in PubMed, 530 citations in OpenAlex.

  1. Article
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  8. Food science & nutrition · 2026
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  11. Review
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  14. Protective potential ofOpen veterinary journal · 2025
    Article
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  20. Review

183 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Walter L MillerDepartment of Pediatrics, School of Medicine, University of California, San Francisco, CA 94143; UCSF Benioff Children's Hospital, San Francisco, CA 94143. Electronic address: wlmlab@ucsf.edu.
Himangshu S BoseDepartment of Biochemistry, Mercer University School of Medicine, Savannah, GA 31404; and; Memorial University Medical Center, Savannah, GA 31404.
UCSF Benioff Children's Hospital · US

Funding

Molecular Biology of Steroidogenic ProteinsR01DK037922 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, WALTER L. · 1987 to 2011
$2.8M
Mechanism of action of steroidogenic acute regulatory protein (StAR)R01HD057876 · NICHD · MERCER UNIVERSITY MACON · PI BOSE, HIMANGSHU S · 2009 to 2013
$1.5M
NICHD NIH HHS HD-57876NICHD NIH HHS R01 HD057876NIDDK NIH HHS DK-37922NIDDK NIH HHS R01 DK037922
6 · The paper itself

Abstract

Steroid hormones are made from cholesterol, primarily derived from lipoproteins that enter cells via receptor-mediated endocytosis. In endo-lysosomes, cholesterol is released from cholesterol esters by lysosomal acid lipase (LAL; disordered in Wolman disease) and exported via Niemann-Pick type C (NPC) proteins (disordered in NPC disease). These diseases are characterized by accumulated cholesterol and cholesterol esters in most cell types. Mechanisms for trans-cytoplasmic cholesterol transport, membrane insertion, and retrieval from membranes are less clear. Cholesterol esters and "free" cholesterol are enzymatically interconverted in lipid droplets. Cholesterol transport to the cholesterol-poor outer mitochondrial membrane (OMM) appears to involve cholesterol transport proteins. Cytochrome P450scc (CYP11A1) then initiates steroidogenesis by converting cholesterol to pregnenolone on the inner mitochondrial membrane (IMM). Acute steroidogenic responses are regulated by cholesterol delivery from OMM to IMM, triggered by the steroidogenic acute regulatory protein (StAR). Chronic steroidogenic capacity is determined by CYP11A1 gene transcription. StAR mutations cause congenital lipoid adrenal hyperplasia, with absent steroidogenesis, potentially lethal salt loss, and 46,XY sex reversal. StAR mutations initially destroy most, but not all steroidogenesis; low levels of StAR-independent steroidogenesis are lost later due to cellular damage, explaining the clinical findings. Rare P450scc mutations cause a similar syndrome. This review addresses these early steps in steroid biosynthesis.

Indexed as

AnimalsBiological TransportCell MembraneCholesterolDiseaseHumansIntracellular SpaceSteroidsCholesterolSteroids

Identifiers

PMID21976778
PMCPMC3283258
OpenAlexW1963827257

What OpenQuestion holds

Textmetadata
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.