What markers track inflammaging?
Inflammaging is the chronic, low-grade, systemic inflammation that accompanies ageing. This page summarises the markers and mechanisms reported in the current literature, including myokines, interleukins, mitochondrial d
Inflammaging is the term used for the chronic, low-grade, systemic inflammatory state that develops with advancing age. It is not a single analyte but a descriptive category, and the literature does not assign it a sequence, formula or molecular weight; it is defined operationally by patterns of circulating mediators and by the cellular processes that sustain them. Reviews of the field group it alongside mitochondrial dysfunction, cellular senescence, neuromuscular junction degeneration and anabolic resistance as interacting contributors to sarcopenia, the progressive age-related loss of muscle mass, strength and physical performance [3].
The mechanistic work centres on cytokine and myokine signalling, with interleukin-6 (IL-6) among the mediators most consistently discussed in the muscle-brain and muscle-systemic literature [2][3].
Research Studies
Myokines and the muscle-brain axis in older adults
A narrative review synthesised mechanistic and translational evidence on how skeletal muscle communicates with the ageing brain through myokines and exerkines. The mediators named include irisin/FNDC5, brain-derived neurotrophic factor (BDNF), IL-6, insulin-like growth factor-1 (IGF-1), cathepsin B and growth differentiation factor-15 (GDF-15). The review proposes that progressive sarcopenia disrupts this signalling and thereby accelerates cognitive impairment, and it notes that sarcopenia and cognitive decline frequently co-occur in older adults [2].
Inflammaging and senescence markers in sarcopenia
A separate review examined biomarkers and early mechanisms of sarcopenia and assigned central roles to mitochondrial dysfunction, inflammaging, cellular senescence and neuromuscular degeneration. It reports that sarcopenia is currently understood to arise from complex interactions among these processes rather than from a single lesion, and that this complexity has limited the development of early diagnostic strategies and targeted therapies [3].
Circulating interleukins and antioxidant capacity in elderly cohorts
A registered study characterises glucose metabolism and inflammaging in subjects aged 70 years and older. It compares healthy, sarcopenic, diabetic and diabetic/sarcopenic groups and correlates patterns of insulin secretion and sensitivity with muscle quality and quantity. The stated aim is to identify an oxidative/inflammatory signature — circulating interleukins and myokines, together with plasma antioxidant capacity — specific to the sarcopenic phenotype and related to muscle insulin resistance [6].
Lipid-soluble nutrients and the heart-brain-bone framework
A review of omega-3, vitamin D3 and vitamin K2 organises evidence from three separate studies around a proposed "Heart-Brain-Bone" axis, linking cardiovascular disease, neurocognitive decline and osteoporotic bone loss through shared regulators of calcium trafficking, inflammation resolution, vascular integrity and inflammaging. The authors describe the axis as an integrative conceptual framework rather than a validated physiological entity, and state that it has no agreed diagnostic criteria or demonstrated modifiability [1].
Dietary micronutrients and inflammaging in cardiovascular risk
A registered study builds on evidence associating fruit and vegetable consumption with reduced cardiac risk, proposing mediation through blood pressure, platelet function and vascular reactivity. It notes that certain vitamins and polyphenols in fruits and vegetables have antioxidant and anti-inflammatory effects and influence immune cell function, and it cites prior work on omega-3 fatty acids, cardiovascular effects, blood lipid regulation and inflammatory response [5].
Surgical stress and damage-associated molecular patterns
A registered trial in older patients undergoing coronary artery bypass grafting describes the surgical stress response in mechanistic terms: systemic epinephrine rising 33-fold and norepinephrine 3-fold, local tissue injury producing sterile inflammation, release of damage-associated molecular patterns (DAMPs), neutrophil activation, and downstream cytokine, complement and coagulation changes. Nociceptor activation is described as driving a neurometabolic response involving the sympathetic nervous system and the hypothalamus-pituitary axis [4].
Markers reported across tissue-specific ageing reviews
Several reviews extend inflammaging markers beyond muscle. One frames chronic, largely mutation-independent overactivation of the DNA damage response as an upstream integrating node in ageing, dysregulating tumour-suppressor networks [7]. Another describes vascular ageing in intracranial aneurysm as driven by cellular senescence, chronic inflammation and haemodynamic stress [8]. A third lists telomere attrition, mitochondrial dysfunction and epigenetic drift among the molecular signatures of chronological skin ageing [9]. A fourth outlines ovarian ageing via an ovarian-systemic axis, in which genomic instability, epigenetic shifts and mitochondrial and proteostasis damage may trigger senescence-associated secretory phenotype (SASP)-related inflammaging and fibrosis [10].
Comparison of marker classes reported
| Marker class | Examples reported | Context in the evidence |
|---|---|---|
| Myokines / exerkines | Irisin/FNDC5, BDNF, IL-6, IGF-1, cathepsin B, GDF-15 | Muscle-brain axis in ageing and sarcopenia [2] |
| Circulating interleukins | Interleukins (unspecified panel) | Elderly cohorts, correlated with muscle insulin resistance [6] |
| Plasma antioxidant capacity | Not specified | Proposed oxidative/inflammatory signature of sarcopenia [6] |
| Damage-associated molecular patterns | DAMPs | Surgical stress response in older CABG patients [4] |
| Cellular senescence / SASP | SASP-related mediators | Vascular, ovarian and skin ageing reviews [8][9][10] |
If you are reading this for personal health reasons
The materials described here are supplied for laboratory research use only. We do not provide dosing information, medical guidance or recommendations for personal use. Anyone considering a compound for themselves should consult a licensed clinician.
Sources
- [1] Beyond Bone Health: Exploring the "Heart-Brain-Bone" Axis Modulated by Lipid-Soluble Nutrients (Omega-3, Vitamin D3, and Vitamin K2) — https://europepmc.org/article/PMC/PMC13516505
- [2] Myokines as molecular mediators of the muscle-brain axis — https://pubmed.ncbi.nlm.nih.gov/42520997/
- [3] Biomarkers and Early Mechanisms of Sarcopenia — https://europepmc.org/article/PMC/PMC13411428
- [4] Alpha Ketoglutarate Enhances Geroprotection In Surgery (AEGIS) — https://clinicaltrials.gov/study/NCT07031128
- [5] Cardiovascular and InflammAging Study — https://clinicaltrials.gov/study/NCT04763291
- [6] Glucose Metabolism, Muscle Mass/Function and Inflammation in the Elderly — https://clinicaltrials.gov/study/NCT02426073
- [7] The guardian paradox: DNA damage response overactivation as an integrative driver of aging — https://pubmed.ncbi.nlm.nih.gov/42684403/
- [8] Intracranial aneurysms as a manifestation of premature vascular aging — https://pubmed.ncbi.nlm.nih.gov/42660465/
- [9] Decoding the multidimensional landscape of skin aging — https://pubmed.ncbi.nlm.nih.gov/42640108/
- [10] Ovarian aging and systemic health — https://pubmed.ncbi.nlm.nih.gov/42607669/