Evidence map›Paper›PMID 36527064›Full record

ReviewLipids in health and disease2022

PCSK9 inhibition and cholesterol homeostasis in insulin producing β-cells.

Günter Päth, Nikolaos Perakakis, Christos S Mantzoros, Jochen Seufert

Open access · goldAbstract readReview
In one paragraph

Review in Lipids in health and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

8 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Reducing LDL-Cholesterol to Very Low Levels: Sailing Between Established Benefits and Potential Risks.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. 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

4 authors at 2 institutions in 2 countries.

Günter PäthDivision of Endocrinology and Diabetology, Department of Medicine II, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany, Hugstetter Str. 55, Freiburg, Germany. guenter.paeth@uniklinik-freiburg.de.
Nikolaos PerakakisDivision of Metabolic and Vascular Medicine, Department of Internal Medicine III, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Christos S MantzorosDivision of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Jochen SeufertDivision of Endocrinology and Diabetology, Department of Medicine II, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany, Hugstetter Str. 55, Freiburg, Germany.
Harvard University · USUniversity of Freiburg · DE

Funding

Deutsche Diabetes Gesellschaft Projektförderung to GP
6 · The paper itself

Abstract

Low-density lipoprotein cholesterol (LDL-C) plays a central role in the pathology of atherosclerotic cardiovascular disease. For decades, the gold standard for LDL-C lowering have been statins, although these drugs carry a moderate risk for the development of new-onset diabetes. The inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) have emerged in the last years as potential alternatives to statins due to their high efficiency and safety without indications for a diabetes risk so far. Both approaches finally eliminate LDL-C from bloodstream by upregulation of LDL receptor surface expression. Due to their low antioxidant capacity, insulin producing pancreatic β-cells are sensitive to increased lipid oxidation and related generation of reactive oxygen species. Thus, PCSK9 inhibition has been argued to promote diabetes like statins. Potentially, the remaining patients at risk will be identified in the future. Otherwise, there is increasing evidence that loss of circulating PCSK9 does not worsen glycaemia since it is compensated by local PCSK9 expression in β-cells and other islet cells. This review explores the situation in β-cells. We evaluated the relevant biology of PCSK9 and the effects of its functional loss in rodent knockout models, carriers of LDL-lowering gene variants and PCSK9 inhibitor-treated patients.

Indexed as

Hydroxymethylglutaryl-CoA Reductase InhibitorsInsulinsCholesterol, LDLHomeostasisProprotein Convertase 9Cholesterol, LDLHydroxymethylglutaryl-CoA Reductase InhibitorsInsulinsPCSK9 protein, humanProprotein Convertase 9Glucose homeostasisInsulin secretionKnockout modelsLoss of function gene variantsPancreatic β-cellsPCSK9 inhibitors

Identifiers

PMID36527064
PMCPMC9756761
OpenAlexW4312066210

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.