Evidence map›Paper›PMID 35017717›Full record

ReviewCellular & molecular immunology2022

Reprogramming cholesterol metabolism in macrophages and its role in host defense against cholesterol-dependent cytolysins.

Min-Sub Lee, Steven J Bensinger

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
17.2field-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

57 citing papers in PubMed, 85 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Single-cell transcriptomics reveal alveolar macrophage-specific responses in single-hit ozone exposure model in mice.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  8. Article
  9. Article
  10. Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Protective Role ofMicroorganisms · 2025
    Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Min-Sub LeeDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.
Steven J BensingerDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA. sbensinger@mednet.ucla.edu.ORCID http://orcid.org/0000-0002-9657-4206
University of California, Los Angeles · US

Funding

Understanding the Influence of Lipid Homeostasis on T cell FunctionP01HL146358 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FONG, LOREN GI · 2019 to 2023
$11.7M
MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
Investigating the impact of a fatty acid-cRel inflammatory circuit in atherosclerosisR01HL157710 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BENSINGER, STEVEN J · 2021 to 2024
$2.3M
NHLBI NIH HHS P01 HL146358NHLBI NIH HHS R01 HL157710NIAID NIH HHS T32 AI007323
6 · The paper itself

Abstract

Cholesterol is a critical lipid for all mammalian cells, ensuring proper membrane integrity, fluidity, and biochemical function. Accumulating evidence indicates that macrophages rapidly and profoundly reprogram their cholesterol metabolism in response to activation signals to support host defense processes. However, our understanding of the molecular details underlying how and why cholesterol homeostasis is specifically reshaped during immune responses remains less well understood. This review discusses our current knowledge of cellular cholesterol homeostatic machinery and introduces emerging concepts regarding how plasma membrane cholesterol is partitioned into distinct pools. We then discuss how proinflammatory signals can markedly reshape the cholesterol metabolism of macrophages, with a focus on the differences between MyD88-dependent pattern recognition receptors and the interferon signaling pathway. We also discuss recent work investigating the capacity of these proinflammatory signals to selectively reshape plasma membrane cholesterol homeostasis. We examine how these changes in plasma membrane cholesterol metabolism influence sensitivity to a set of microbial pore-forming toxins known as cholesterol-dependent cytolysins that specifically target cholesterol for their effector functions. We also discuss whether lipid metabolic reprogramming can be leveraged for therapy to mitigate tissue damage mediated by cholesterol-dependent cytolysins in necrotizing fasciitis and other related infections. We expect that advancing our understanding of the crosstalk between metabolism and innate immunity will help explain how inflammation underlies metabolic diseases and highlight pathways that could be targeted to normalize metabolic homeostasis in disease states.

Indexed as

CholesterolCytotoxinsAnimalsCell MembraneImmunity, InnateMacrophagesMammalsCholesterolCytotoxinsCholesterolInnate ImmunityMacrophagesMetabolism

Identifiers

PMID35017717
PMCPMC8891295
OpenAlexW4206405516

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.