Evidence map›Paper›PMID 40342966›Full record

ArticlebioRxiv : the preprint server for biology2025

Postoperative Stress Accelerates Atherosclerosis through Inflammatory Remodeling of the HDL Proteome and Impaired Reverse Cholesterol Transport.

Dominique M Boucher, Valerie Rochon, Thomas Laval, Victoria Lorant, Abigail Carter, Christina Emerton, Nathan Joyce, Nysa Vinayak, Marlena Scaffidi, Rebecca C Auer and 2 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Dominique M BoucherDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.ORCID 0000-0003-2223-0117
Valerie RochonDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.
Thomas LavalDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.ORCID 0000-0002-9359-2783
Victoria LorantDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.
Abigail CarterSaha Cardiovascular Research Center and Department of Physiology, University of Kentucky, 741 South Limestone, Lexington, KY, 40536-0509, USA.
Christina EmertonUniversity of Ottawa Heart Institute, 40 Ruskin St, Ottawa, ON, K1Y 4W7, Canada.
Nathan JoyceDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.
Nysa VinayakUniversity of Ottawa Heart Institute, 40 Ruskin St, Ottawa, ON, K1Y 4W7, Canada.
Marlena ScaffidiDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.
Rebecca C AuerDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.
Scott M GordonSaha Cardiovascular Research Center and Department of Physiology, University of Kentucky, 741 South Limestone, Lexington, KY, 40536-0509, USA.ORCID 0000-0001-9532-032X
Mireille I OuimetDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd., Ottawa, ON, K1H 8M5, Canada.ORCID 0000-0002-6831-5047

Funding

Functional Interactions Between Lipoproteins and Protease Inhibitors in AtherosclerosisR01HL171111 · NHLBI · UNIVERSITY OF KENTUCKY · PI Scott M Gordon · 2024 to 2026
$1.9M
NHLBI NIH HHS R01 HL171111
6 · The paper itself

Abstract

backgroundOver 10 million patients undergoing non-cardiac surgery annually experience major cardiovascular complications within 30 days, many due to destabilized atherosclerotic plaques. Reverse cholesterol transport (RCT), a key pathway for cholesterol removal by HDL and apoA-I, is critical in preventing plaque progression. While surgery-induced inflammation is known to impair HDL function, its effects on RCT and plaque stability remain unclear.

methodsTo isolate the impact of surgical inflammation, independent of blood loss, we developed an abdominal laparotomy model in

resultsSurgery significantly reduced RCT for at least 48 hours, paralleled by a drop in cholesterol efflux capacity and inflammatory remodeling of HDL, marked by elevated serum amyloid A (SAA1/2) and reduced apoA-I. Plaques showed a 1.6-fold increase in intracellular lipids and PLIN2 expression at 24 hours post-surgery, with elevated c-Casp-3 indicating lipid-driven apoptosis. Foam cell analysis revealed increased PLIN2 in both CD45

conclusionsSurgical inflammation acutely impairs HDL function and RCT, triggering lipid accumulation, foam cell apoptosis, and accelerated plaque destabilization independent of blood loss. Immediate restoration of apoA-I at the time of surgery, aiming to counteract the acute phase response, may offer a targeted strategy to reduce postoperative cardiovascular risk.

Indexed as

acute phase responseatherosclerosisHDLreverse cholesterol transportsurgery

Identifiers

PMID40342966
PMCPMC12060993

What OpenQuestion holds

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Registered trials

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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.