Study explores the link between ‘inflammaging’ and heart ageing

Inflammaging: when chronic age-related inflammation weakens the heart

The term ‘inflammaging’ refers to a chronic, low-grade inflammation linked to ageing that develops silently, persistently, and without any immediate apparent cause (pathogen, trauma, etc.).

This latent inflammatory state is thought to lead to the functional decline of several organs, including the heart. A recent scientific review, published in 2026, details precisely how inflammaging influences cardiovascular ageing (1).

How does inflammaging affect the ageing of the heart?

Senescent cells, the cause of inflammaging

At the heart of the concept of inflammaging lie senescent cells. These are ‘ageing’ cells that have lost their ability to divide (2). Far from being inert, they remain metabolically active and adopt harmful behaviour. Over time, they accumulate in tissues — including the heart muscle and blood vessels — and disrupt their normal functioning.

SASP: a chronic inflammatory signal

Senescent cells secrete a complex set of molecules known as SASP (Senescence-Associated Secretory Phenotype) (3). This cocktail includes:

• pro-inflammatory cytokines (such as IL-6, TNF-α);
• chemokines;
• extracellular matrix remodelling enzymes;
• growth factors (including GDF-15).

This secretory profile sustains chronic local inflammation and facilitates the spread of senescence to neighbouring cells. Certain SASP markers, such as GDF-15, are also associated with a poor prognosis in several cardiovascular diseases.

Direct effects on the heart and blood vessels

The study highlights the concrete consequences of inflammaging on the cardiovascular system. The following were noted:

• increased vascular stiffness;
• endothelial dysfunction (the inner lining of blood vessels);
• progressive cardiac remodelling.

These changes reduce the blood vessels’ ability to dilate properly, destabilise blood flow and increase the heart’s workload, which in the long term may increase cardiovascular risk (4).

A vicious circle between inflammation and cellular ageing

The review also highlights the existence of a vicious circle between inflammaging and cardiac ageing. Chronic inflammation promotes the emergence of new senescent cells, which, in turn, amplify the inflammatory response via the SASP. This self-perpetuating system directly contributes to accelerating cellular and tissue ageing, particularly in the heart.

Can we intervene in inflammaging and senescent cells?

Targeting senescent cells

Research is increasingly focusing on so-called ‘senolytic’ strategies, aimed at eliminating senescent cells or limiting their harmful effects.

Certain natural compounds are attracting growing interest. One such compound is fisetin, a polyphenol found notably in strawberries, which is being studied for its potential ability to support the self-destruction of damaged cells (including senescent cells) and to activate the autophagy mechanism (which cleanses and recycles cellular waste) (5).

The Fisetin supplement boasts a record-breaking fisetin content (500 mg per 2 capsules).

In the field of cellular longevity, quercetin is also making quite a name for itself. This powerful antioxidant flavonoid supports cardiovascular health by normalising blood pressure and endothelial function, as well as by curbing low-grade inflammation (6).

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It is worth noting that there are synergistic formulas combining several senolytic active ingredients that address the various aspects of cellular senescence.

In addition to quercetin and fisetin, Senolytic Complex contains the most prominent compounds in anti-ageing research: green tea, bromelain, NMN, vitamin C...

Reducing low-grade inflammation

Reducing chronic inflammation amounts to tackling inflammaging at its root. Several natural active ingredients are thought to possess a certain ability to modulate inflammatory pathways.

Research suggests, for example, that apigenin may inhibit the expression of several pro-inflammatory compounds (NF-κB, COX-2, etc.) and mitigate oxidative stress in an inflammatory context. It also appears to have the ability to increase levels of ^NAD+, a key player in cellular metabolism (7-8).

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PEA (palmitoylethanolamide) is a bioactive lipid produced by most of our cells in response to stress. By modulating inflammatory signalling (activation of PPAR-α receptors, interactions with the endocannabinoid system, etc.) and regulating the activity of mast cells (a specific type of immune cell), it may help to limit excessive inflammatory responses (9).

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Supporting cellular and mitochondrial functions

Mitochondria, the energy powerhouses embedded in the cytoplasm of cells, play a role in the synthesis of ATP (cellular energy) and in managing oxidative stress (10). However, as we age, their performance declines: they produce less energy, neutralise free radicals less effectively and provide less support to cellular repair systems. This mitochondrial dysfunction thus appears to be closely linked to inflammaging and cellular senescence.

Supporting their activity is therefore an excellent complementary strategy. And this is where NAD+ comes in! Indeed, this coenzyme supports ATP production, activates sirtuins (enzymes involved in cellular longevity) and works in tandem with PARP enzymes responsible for DNA repair (11). Unfortunately, its levels decline with age.

NAD+ Booster Formula combines the 3 best NAD+ ‘boosters’, including the exclusive ingredient BluNAD Booster™ (a blend of pomegranate fruit peel extract and marigold flower extract).