Evidence map›Paper›PMID 41243886›Full record

ArticleAnatolian journal of cardiology2025

PCSK9 Inhibition Protects Against Myocardial Ischemia-Reperfusion Injury in Type 2 Diabetes Rats Via Suppressing Inflammation and Apoptosis.

Mengjuan Zhang, Fu Liu, Yanbo Gao, Yi He, Shouzheng Bian, Bo Yang, Peiqing Liu, Yanan Zheng, Yan Zhu

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In one paragraph

Article in Anatolian journal of cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Mengjuan ZhangDepartment of Endocrinology, Baotou Central Hospital, Baotou, China.
Fu LiuDepartment of Cardiology, Baotou Central Hospital, Baotou, China.
Yanbo GaoDepartment of Endocrinology, Baotou Central Hospital, Baotou, China.
Yi HeDepartment of Endocrinology, Baotou Central Hospital, Baotou, China.
Shouzheng BianDepartment of Endocrinology, Baotou Central Hospital, Baotou, China.
Bo YangDepartment of Endocrinology, Baotou Central Hospital, Baotou, China.
Peiqing LiuDepartment of Endocrinology, Baotou Central Hospital, Baotou, China.
Yanan ZhengDepartment of Neurology, Baotou Central Hospital, Baotou, China.
Yan ZhuDepartment of Endocrinology, Baotou Central Hospital, Baotou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial ischemia-reperfusion (I/R) injury is aggravated in type 2 diabetes mellitus (T2DM) due to metabolic dysfunction, inflammation, and apoptosis. This study investigated the cardioprotective role of alirocumab, a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, compared with atorvastatin.

methodsType 2 diabetes mellitus was induced in rats by a high-fat/high-sugar diet plus streptozotocin injection, followed by myocardial I/R through transient ligation of the left anterior descending artery. Rats (n = 6/group) were randomized into Control, non-diabetic I/R, T2DM + I/R, T2DM + I/R + alirocumab, and T2DM + I/R + atorvastatin groups. Alirocumab (10 mg/kg/week, intraperitoneal injection) or atorvastatin (10 mg/kg/day, oral) was administered for 21 days. Outcomes included lipid deposition, myocardial fibrosis, metabolic parameters, inflammatory cytokines, apoptosis, and expression of PCSK9, nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), and Caspase-3, assessed by histology, enzyme-linked immunosorbent assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, western blotting, and quantitative reverse transcription polymerase chain reaction.

resultsNon-diabetic I/R rats showed increased lipid accumulation, fibrosis, inflammation, and apoptosis compared with controls, while these effects were markedly exacerbated in T2DM + I/R, confirming the amplifying effect of diabetes. Both alirocumab and atorvastatin significantly reduced lipid accumulation, improved hepatic and renal function, lowered free fatty acids and HbA1c, and restored insulin and C-peptide levels (P < .001). Treatments also decreased pro-inflammatory cytokines (interleukin-1β [IL-1β], interleukin-6 [IL-6], tumor necrosis factor-α [TNF-α]), inhibited NLRP3 inflammasome activation, reduced myocardial apoptosis and caspase-3 activity, and downregulated myocardial PCSK9, NLRP3, and caspase-3 expression. Protective effects were comparable between alirocumab and atorvastatin.

conclusionAlirocumab and atorvastatin effectively attenuated myocardial I/R injury in T2DM by modulating lipid metabolism, inflammation, and apoptosis. Diabetes substantially intensified I/R-induced cardiac injury, underscoring the importance of metabolic control in cardioprotection. #Means they contributed equally to the article.

Indexed as

Antibodies, Monoclonal, HumanizedDiabetes Mellitus, Type 2Myocardial Reperfusion InjuryPCSK9 InhibitorsAnimalsApoptosisAtorvastatinDiabetes Mellitus, ExperimentalDisease Models, AnimalInflammationMaleProprotein Convertase 9Random AllocationRatsRats, Sprague-DawleyalirocumabAntibodies, Monoclonal, HumanizedAtorvastatinPCSK9 InhibitorsPCSK9 protein, ratProprotein Convertase 9

Identifiers

PMID41243886
PMCPMC12979069

What Socratic holds

Texttitle and abstract
LicenceCC BY-NC
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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 Socratic graph.