Evidence map›Paper›PMID 39622633›Full record

ArticleBMB reports2024

Targeting proprotein convertase subtilisin/kexin type 7 in macrophages as a therapeutic strategy to mitigate myocardial infarction-induced inflammation.

Shin Hye Moon, Inyoung Chung, Na Hyeon Yoon, Jing Jin, Hyae Yon Kweon, Won Kee Yoon, Nabil G Seidah, Goo Taeg Oh

Abstract read
In one paragraph

Article in BMB reports, 2024. 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

8 authors.

Shin Hye MoonHeart-Immune-Brain Network Research Center, Department of Life Sciences, Ewha Womans University, Seoul 03760, Korea.
Inyoung ChungHeart-Immune-Brain Network Research Center, Department of Life Sciences, Ewha Womans University, Seoul 03760, Korea.
Na Hyeon YoonHeart-Immune-Brain Network Research Center, Department of Life Sciences, Ewha Womans University, Seoul 03760, Korea.
Jing JinHeart-Immune-Brain Network Research Center, Department of Life Sciences, Ewha Womans University, Seoul 03760, Korea.
Hyae Yon KweonHeart-Immune-Brain Network Research Center, Department of Life Sciences, Ewha Womans University, Seoul 03760, Korea.
Won Kee YoonKorea Research Institute of Bioscience & Biotechnology, Laboratory Animal Resource Center, Cheongju 28116, Korea.
Nabil G SeidahLaboratory of Biochemical Neuroendocrinology, Montreal Clinical Research Institute (IRCM), Montreal, Quebec H2W 1R7, Canada.
Goo Taeg OhHeart-Immune-Brain Network Research Center, Department of Life Sciences, Ewha Womans University, Seoul 03760, Korea; Imvastech Inc., Seoul 03760, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI), a major form of coronary artery disease (CAD), triggers a severe inflammatory response in the heart, resulting in increased cell death and adverse ventricular remodeling. Despite treatment advancements, MI remains a significant risk factor for heart failure, underscoring the necessity for a more in-depth exploration of immune cell mechanisms. Proprotein convertase subtilisin/kexin type 7 (PCSK7), expressed in various tissues and immune cells, has been implicated in cardiovascular disease, yet its specific role in cardiac immune cells remains poorly understood. This study aimed to elucidate the role of PCSK7 in MI-related inflammation. Our findings indicate that PCSK7 deficiency reduces circulating cholesterol levels, potentially mitigating infarct injury and improving cardiac function by modulating immune cells. Additionally, PCSK7 promotes macrophage activation and lipid uptake at the ischemic site, intensifying the pathology. We also observed that PCSK7 activates the TNF-α/JNK signaling pathway in macrophages intracellularly, amplifying the inflammatory response. Therefore, targeting PCSK7 in macrophages could help mitigate post-MI inflammation, alleviate disease severity, and offer novel therapeutic strategies for patients with CAD. [BMB Reports 2024; 57(12): 553-558].

Indexed as

InflammationMacrophagesMyocardial InfarctionAnimalsHumansMacrophage ActivationMaleMiceMice, Inbred C57BLSignal TransductionTumor Necrosis Factor-alphaTumor Necrosis Factor-alpha

Identifiers

PMID39622633
PMCPMC11693601

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.