ArticleAging2012
Inflammaging: disturbed interplay between autophagy and inflammasomes.
Article in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 267 papers, 3 of them syntheses that pooled it.
What it found
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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
267 citing papers in PubMed, 3 syntheses or guidelines pooled it, 480 citations in OpenAlex.
- Pooled it
- Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.Frontiers in immunology · 2022Pooled it
- Pooled it
- Infusion of young donor plasma components in older patients modifies the immune and inflammatory response to surgical tissue injury: a randomized clinical trial.Journal of translational medicine · 2025Trial
- Effects of Interleukin-1β Inhibition on Incident Anemia: Exploratory Analyses From a Randomized Trial.Annals of internal medicine · 2020Trial
- Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects.Aging · 2017Trial
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- A Biological Disease-Staging Model of Polyendocrine Metabolic Ovarian Syndrome: From Plasticity-Dominant States to Pathological Remodeling.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Identification of Age-Associated Upstream Regulators to Promote Neuronal Resilience in HD Patient-Derived Neurons.Neuroscience bulletin · 2026Article
- Understanding and addressing resistance to IMiDs immunomodulatory compounds in multiple myeloma.The FEBS journal · 2026Review
- Targeting inflammaging in Alzheimer's disease: molecular pathways and emerging pharmacotherapies.Inflammopharmacology · 2026Review
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- AMPK-NLRP3 Inflammasome Crosstalk: Structural Insights, Molecular Mechanisms, and Therapeutic Implications for Inflammation and Neuroinflammation.Molecular neurobiology · 2026Review
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- CD8Science China. Life sciences · 2026Review
- Dietary Polyphenols in Aging: A Systems-Level Perspective on Mitochondrial Quality Control and Microbiome Interactions.International journal of molecular sciences · 2026Review
- Aging at the Crossroads of Cuproptosis and Ferroptosis: From Molecular Pathways to Age-Related Pathologies and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Mechanistic intersections of empagliflozin and nebivolol in aging-associated redox and inflammatory pathways.Frontiers in pharmacology · 2026Review
- Mitochondrial medicine in obesity: a scoping review.Open medicine (Warsaw, Poland) · 2026Review
- Non-thermal processing of polyphenol- and carotenoid-rich green leafy vegetables for healthy aging: effects on antioxidant properties and bioavailability.Frontiers in nutrition · 2026Review
207 more citing papers are in PubMed but not listed here.
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammaging refers to a low-grade pro-inflammatory phenotype which accompanies aging in mammals. The aging process is associated with a decline in autophagic capacity which impairs cellular housekeeping, leading to protein aggregation and accumulation of dysfunctional mitochondria which provoke reactive oxygen species (ROS) production and oxidative stress. Recent studies have clearly indicated that the ROS production induced by damaged mitochondria can stimulate intracellular danger-sensing multiprotein platforms called inflammasomes. Nod-like receptor 3 (NLRP3) can be activated by many danger signals, e.g. ROS, cathepsin B released from destabilized lysosomes and aggregated proteins, all of which evoke cellular stress and are involved in the aging process. NLRP3 activation is also enhanced in many age-related diseases, e.g. atherosclerosis, obesity and type 2 diabetes. NLRP3 activates inflammatory caspases, mostly caspase-1, which cleave the inactive precursors of IL-1β and IL-18 and stimulate their secretion. Consequently, these cytokines provoke inflammatory responses and accelerate the aging process by inhibiting autophagy. In conclusion, inhibition of autophagic capacity with aging generates the inflammaging condition via the activation of inflammasomes, in particular NLRP3. We will provide here a perspective on the current research of the ROS-dependent activation of inflammasomes triggered by the decline in autophagic cleansing of dysfunctional mitochondria.
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What OpenQuestion 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 OpenQuestion graph.