Narrative review of therapies targeting inflammaging in age-related multimorbidity
This narrative review describes therapies aimed at mechanisms of inflammaging — senescent cells and their secretory factors, NAD⁺ decline and inflammasome activation — plus anti-inflammatory drugs and lifestyle measures; it notes that limited validated biomarkers, complex trial designs and missing long-term safety data hinder clinical translation. [1]
Automatic summary · not editorially reviewed
The key findings
The review states that much of the chronic multimorbidity burden in the aging population is driven by inflammaging, a persistent low-grade inflammatory state recognized as a hallmark of biological aging. [1]
Senolytic combinations such as dasatinib plus quercetin and the flavonoid fisetin reduced circulating senescence-associated secretory factors in early studies. [1]
The review notes that clinical translation is challenging because validated biomarkers are limited, trial designs are complex and long-term safety data are still needed. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- People affected by chronic multimorbidity in the global aging population, as discussed in the review
- Summary based on
- Study abstract
- Original publication
- September 19, 2026
Inflammaging as driver of multimorbidity
The review states that the global aging population faces a growing burden of chronic multimorbidity, much of it driven by inflammaging. It defines inflammaging as a persistent, low-grade inflammatory state recognized as a hallmark of biological aging. The review then examines therapeutic strategies targeting key mechanisms of inflammaging, focusing on cellular senescence and the senescence-associated secretory phenotype, NAD⁺ decline and inflammasome activation.
Supporting source [1]
Senolytics, senomorphics and NAD⁺ precursors
Senolytic therapies designed to eliminate senescent cells have entered early-phase clinical trials. Combinations such as dasatinib plus quercetin and the flavonoid fisetin reduced circulating senescence-associated secretory factors in early studies. Senomorphic agents such as rapamycin and Janus kinase inhibitors instead suppress production of these factors while preserving cell viability. Supplementation with NAD⁺ precursors such as nicotinamide riboside and nicotinamide mononucleotide showed beneficial effects on vascular function and metabolic health in early human studies; inhibiting the NAD⁺-consuming enzyme CD38 is described as a complementary strategy.
Supporting source [1]
Anti-inflammatory drugs, lifestyle and translation gaps
Targeted anti-inflammatory biologics against cytokines such as IL-1β, IL-6 and TNF-α showed clinical benefits in cardiovascular disease, supporting inflammation-targeted therapy. Repurposed metabolic medications including metformin, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists also show anti-inflammatory effects. Evidence-based lifestyle interventions such as caloric restriction, regular exercise and Mediterranean dietary patterns remain important complementary strategies. The review notes that clinical translation is challenging because validated biomarkers are limited, trial designs are complex and long-term safety data are still needed.
Supporting source [1]
How to interpret this
This is an abstract of a narrative review; the full text was not reviewed. The abstract reports no sample sizes, follow-up durations or effect estimates, and the cited early studies and trials are described only in general terms.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Ayoub NR. · europepmc.org · September 19, 2026