Evidence map›Paper›PMID 25879284›Full record

ReviewImmunological reviews2015

Drivers of age-related inflammation and strategies for healthspan extension.

Emily L Goldberg, Vishwa Deep Dixit

Registry-linked trialAbstract readReview
In one paragraph

Review in Immunological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07774260 (Efficacy Validation of Deep Microspicule Cream for Anti-aging and Whitening on Mature Skin), which is not on this map. Cited by 161 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 2 pooled it
9.5field-weighted citation impact, top 1% of its field
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.

NCT07774260 nanot yet recruitingnot on this mapstarted 2026, after this paper: background citation

Efficacy Validation of Deep Microspicule Cream for Anti-aging and Whitening on Mature Skin

TypeinterventionalSponsorChung Shan Medical UniversityRan2026 to 2026Enrolled10ConditionsEfficacy Validation of Deep Microspicule Cream for Anti-aging and Whitening on Mature SkinArmsDeep Microspicule Cream
3 · Its place in the literature

Who cites it

161 citing papers in PubMed, 2 syntheses or guidelines pooled it, 271 citations in OpenAlex.

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101 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Emily L GoldbergSection of Comparative Medicine, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
Vishwa Deep Dixit
Yale University · US

Funding

Thymic adipogenesis and age-related thymic demiseR01AI105097 · NIAID · YALE UNIVERSITY · PI DIXIT, VISHWA DEEP · 2015 to 2018
$1.9M
Inflammasomes and the mechanism of thymic demise in agingR01AG043608 · NIA · YALE UNIVERSITY · PI DIXIT, VISHWA DEEP · 2013 to 2017
$1.8M
Impact of Obesity and Weight-Loss Interventions on Immune-Surveillance MechanismsR01DK090556 · NIDDK · YALE UNIVERSITY · PI DIXIT, VISHWA DEEP · 2011 to 2014
$1.6M
Impact of CR on inflammasome driven immune-metabolic interactions.R01AG045712 · NIA · YALE UNIVERSITY · PI DIXIT, VISHWA DEEP · 2013 to 2014
$525k
Thymic adipogenesis and age-related thymic demiseR56AI105097 · NIAID · YALE UNIVERSITY · PI DIXIT, VISHWA DEEP · 2013 to 2013
$348k
NIAID NIH HHS AI105097NIAID NIH HHS R01 AI105097NIAID NIH HHS R56 AI105097NIA NIH HHS AG043608NIA NIH HHS AG045712NIA NIH HHS R01 AG043608NIA NIH HHS R01 AG045712NIDDK NIH HHS DK090556NIDDK NIH HHS R01 DK090556
6 · The paper itself

Abstract

Aging is the greatest risk factor for the development of chronic diseases such as arthritis, type 2 diabetes, cardiovascular disease, kidney disease, Alzheimer's disease, macular degeneration, frailty, and certain forms of cancers. It is widely regarded that chronic inflammation may be a common link in all these age-related diseases. This raises the question, can one alter the course of aging and potentially slow the development of all chronic diseases by manipulating the mechanisms that cause age-related inflammation? Emerging evidence suggests that pro-inflammatory cytokines interleukin-1 (IL-1) and IL-18 show an age-dependent regulation implicating inflammasome-mediated caspase-1 activation in the aging process. The Nod-like receptor (NLR) family of innate immune cell sensors, such as the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome controls the caspase-1 activation in myeloid-lineage cells in several organs during aging. The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age. Interestingly, reduction in NLRP3-mediated inflammation prevents age-related insulin resistance, bone loss, cognitive decline, and frailty. NLRP3 is a major driver of age-related inflammation and therefore dietary or pharmacological approaches to lower aberrant inflammasome activation holds promise in reducing multiple chronic diseases of age and may enhance healthspan.

Indexed as

AgingAnimalsCarrier ProteinsCaspase 1HumansInflammationInterleukin-1Myeloid CellsNLR Family, Pyrin Domain-Containing 3 ProteinCarrier ProteinsCaspase 1Interleukin-1NLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanadipose tissuecytokinesIL-1IL-18inflammasomemacrophageNLRP3sarcopeniasenescence

Identifiers

PMID25879284
PMCPMC4400872
OpenAlexW1995481571

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.