Review proposes multi-organ crosstalk framework for cardiometabolic aging
This review reframes cardiac senescence as a systemic result of pathological crosstalk between the heart and peripheral metabolic organs, and proposes nodal points to block that crosstalk and delay cardiovascular aging. [1]
Automatic summary · not editorially reviewed
The key findings
The review replaces an organ-centric view with four multi-organ crosstalk axes involving the heart. [1]
The described mediators converge on oxidative stress, impaired autophagy and cellular senescence, acting synergistically through the circulation. [1]
The authors propose senolytics, myokine mimetics, gut microbiota modulation, RAAS/SGLT2 inhibitors and integrated lifestyle strategies as nodal points. [1]
The source at a glance
- Study type / format
- Review (abstract only)
- Population / context
- Review of cardiac aging and peripheral metabolic organs; no human participants described.
- Summary based on
- Study abstract
- Original publication
- August 1, 2026
Four organ-heart axes replace organ-centric view
The review sets aside the traditional organ-centric perspective and builds an integrated framework around multi-organ crosstalk axes: epicardial adipose tissue-heart, skeletal muscle-heart, gut-heart and kidney-heart. For each axis it describes local molecular mediators, including inflammatory cytokines, lipotoxic metabolites, microbiota-derived compounds such as trimethylamine N-oxide (TMAO), renin-angiotensin-aldosterone system (RAAS) effectors and extracellular vesicle cargoes.
Supporting source [1]
Signals converge on shared senescence pathways
According to the review, these mediators converge onto common pathways of oxidative stress, impaired autophagy and cellular senescence. The signals are described as acting synergistically through the circulation, converting local organ dysfunction into systemic cardiac aging. The authors therefore describe aging as potentially modifiable multi-organ crosstalk.
Supporting source [1]
Proposed nodal points aim to delay cardiovascular aging
The review proposes emerging nodal points to block pathological crosstalk and delay cardiovascular aging: senolytics, myokine mimetics, gut microbiota modulation, RAAS/sodium-glucose cotransporter 2 (SGLT2) inhibitors and integrated lifestyle strategies. These are presented as a research framework that shifts focus from isolated organs to systemic multi-organ crosstalk, not as tested treatments.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. The proposed nodal points are a framework, not validated treatments, and the abstract reports no study design, sample or outcome data.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Zhang S, Xu C, Song Y, Zhang X. · europepmc.org · August 1, 2026