Evidence map›Paper›PMID 39877020›Full record

ReviewFrontiers in cardiovascular medicine2024

Mechanisms of inflammatory microenvironment formation in cardiometabolic diseases: molecular and cellular perspectives.

Menghua Liu, Rumeng Chen, Zhiwei Zheng, Shuling Xu, Chunyan Hou, Yining Ding, Mengling Zhang, Meihua Bao, Binsheng He, Sen Li

Abstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
–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

22 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

10 authors.

Menghua Liu *School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Rumeng Chen *School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Zhiwei Zheng *School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Shuling Xu *School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Chunyan Hou *School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Yining DingSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Mengling ZhangSchool of Stomatology, Changsha Medical University, Changsha, China.
Meihua BaoHunan key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, School of Pharmaceutical Science, Changsha Medical University, Changsha, China.
Binsheng HeHunan key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, School of Pharmaceutical Science, Changsha Medical University, Changsha, China.
Sen LiSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiometabolic diseases (CMD) are leading causes of death and disability worldwide, with complex pathophysiological mechanisms in which inflammation plays a crucial role. This review aims to elucidate the molecular and cellular mechanisms within the inflammatory microenvironment of atherosclerosis, hypertension and diabetic cardiomyopathy. In atherosclerosis, oxidized low-density lipoprotein (ox-LDL) and pro-inflammatory cytokines such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α) activate immune cells contributing to foam cell formation and arterial wall thickening. Hypertension involves the activation of the renin-angiotensin system (RAS) alongside oxidative stress-induced endothelial dysfunction and local inflammation mediated by T cells. In diabetic cardiomyopathy, a high-glucose environment leads to the accumulation of advanced glycation end products (AGEs), activating the Receptor for Advanced Glycation Endproducts (RAGE) and triggering inflammatory responses that further damage cardiac and microvascular function. In summary, the inflammatory mechanisms in different types of metabolic cardiovascular diseases are complex and diverse; understanding these mechanisms deeply will aid in developing more effective individualized treatment strategies.

Indexed as

atherosclerosiscardiometabolic diseasesdiabetic cardiomyopathyhypertensioninflammatory microenvironment

Identifiers

PMID39877020
PMCPMC11772298

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.