Evidence map›Paper›PMID 42939931›Full record

ReviewAntioxidants (Basel, Switzerland)2026

The Senescence-Malignancy Axis: An Inflammaging Perspective.

Irene Patrono, Margherita Sonnessa, Marco Trerotola, Anna Maria Giudetti, Simona De Summa, Francesco Alfredo Zito, Concetta Saponaro, Daniele Vergara

Abstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Irene PatronoPathology Department, IRCCS Istituto Tumori "Giovanni Paolo II", 70124 Bari, Italy.
Margherita SonnessaPathology Department, IRCCS Istituto Tumori "Giovanni Paolo II", 70124 Bari, Italy.
Marco TrerotolaDepartment of Medical, Oral and Biotechnological Sciences, University "G. D'Annunzio" of Chieti-Pescara, 66100 Chieti, Italy.ORCID 0000-0003-1855-7002
Anna Maria GiudettiDepartment of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, 73100 Lecce, Italy.ORCID 0000-0002-9204-040X
Simona De SummaMolecular Diagnostics and Pharmacogenetics Unit, IRCCS Istituto Tumori "Giovanni Paolo II", 70124 Bari, Italy.ORCID 0000-0001-9607-3754
Francesco Alfredo ZitoPathology Department, IRCCS Istituto Tumori "Giovanni Paolo II", 70124 Bari, Italy.ORCID 0000-0003-4140-4020
Concetta SaponaroPathology Department, IRCCS Istituto Tumori "Giovanni Paolo II", 70124 Bari, Italy.ORCID 0000-0002-8196-3583
Daniele VergaraDepartment of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, 73100 Lecce, Italy.ORCID 0000-0002-2396-7674

Funding

Ministry of Health Italian Ministry of Health for Ricerca Corrente 2026 (F.A.Z).
6 · The paper itself

Abstract

The transition from physiological cellular senescence to malignancy is not an isolated event, but a gradual, systemic remodeling of the biological landscape orchestrated by the persistent state of inflammaging. As detailed in this review, senescent populations do not remain passive. Through the chronic deployment of the senescence-associated secretory phenotype (SASP), they actively dismantle tissue architecture and convert healthy organs into a highly permissive pro-tumorigenic "soil". This cross-talk is mediated by a complex network of signaling cascades including the IL-1 family, IL-6 and TNF-α, CXCL10 and CCL2-CCR2 chemokine axes, and MMPs. Crucially, this cellular decay is reinforced by a profound metabolic shift toward a hyper-glycolytic "metabolic SASP," where extracellular lactate accumulation and prostaglandin synthesis permanently sustain the senescent state. Cellular senescence through the persistent accumulation of senescent cells and the accompanying age-related decline in immune surveillance drive "inflammaging", a chronic, low-grade systemic inflammation that serves as a primary mechanistic bridge fueling the aging-cancer cycle.

Indexed as

aginggeroncologyimmune-senescenceinflammaging

Identifiers

PMID42939931
PMCPMC13701857

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.