ReviewNature reviews. Cardiology2025
Haematometabolism rewiring in atherosclerotic cardiovascular disease.
Review in Nature reviews. Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Integrative statistical genetics prioritizes candidate ASCVD susceptibility genes across tissues.Molecular medicine (Cambridge, Mass.) · 2026Article
- Precision medicine for atherosclerotic cardiovascular disease: Integrative genomics maps risk loci and AI-predicted functional consequences.Clinical and translational medicine · 2026Article
- Association of Genetic Liability to Psychiatric Disorders with Peripheral Metabolic Dysregulation.medRxiv : the preprint server for health sciences · 2026Article
- Slc7a7 licenses macrophage glutaminolysis for restorative functions in atherosclerosis.Nature metabolism · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerotic cardiovascular diseases are the most frequent cause of death worldwide. The clinical complications of atherosclerosis are closely linked to the haematopoietic and immune systems, which maintain homeostatic functions and vital processes in the body. The nodes linking metabolism and inflammation are receiving increasing attention because they are inextricably linked to inflammatory manifestations of non-communicable diseases, including atherosclerosis. Although metabolism and inflammation are essential to survival and involve all tissues, we still know little about how these processes influence each other. In an effort to understand these mechanisms, in this Review we explore whether and how potent cardiovascular risk factors and metabolic modifiers of atherosclerosis influence the molecular and cellular machinery of 'haematometabolism' (metabolic-dependent haematopoietic stem cell skewing) and 'efferotabolism' (metabolic-dependent efferocyte reprogramming). These changes might ultimately propagate a quantitative and qualitative drift of the macrophage supply chain and affect the clinical manifestations of atherosclerosis. Refining our understanding of the different metabolic requirements of these processes could open the possibility of developing therapeutics targeting haematometabolism that, in conjunction with improved dietary habits, help rebalance and promote efficient haematopoiesis and efferocytosis and decrease the risk of atherosclerosis complications.
Indexed as
Identifiers
39743562What Socratic holds
Registered trials
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.