Evidence map›Paper›PMID 32358737›Full record

ReviewJournal of endocrinological investigation2020

Molecular basis of ageing in chronic metabolic diseases.

R Spinelli, L Parrillo, M Longo, P Florese, A Desiderio, F Zatterale, C Miele, G Alexander Raciti, F Beguinot

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of endocrinological investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.8field-weighted citation impact, top 4% 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.

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

57 citing papers in PubMed, 92 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

R SpinelliDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
L ParrilloDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
M LongoDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
P FloreseDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
A DesiderioDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
F ZatteraleDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
C MieleDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
G Alexander RacitiDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy.
F BeguinotDepartment of Translation Medicine, Federico II University of Naples, 80131, Naples, Italy. beguino@unina.it.
University of Naples Federico II · ITInstitute for Experimental Endocrinology and Oncology · IT

Funding

Associazione Italiana per la Ricerca sul Cancro-AIRC IG19001INCIPIT program co-funded by the European Union's Horizon 2020 Programme-Marie Skłodowska-Curie Actions 665403
6 · The paper itself

Abstract

aimOver the last decades, the shift in age distribution towards older ages and the progressive ageing which has occurred in most populations have been paralleled by a global epidemic of obesity and its related metabolic disorders, primarily, type 2 diabetes (T2D). Dysfunction of the adipose tissue (AT) is widely recognized as a significant hallmark of the ageing process that, in turn, results in systemic metabolic alterations. These include insulin resistance, accumulation of ectopic lipids and chronic inflammation, which are responsible for an elevated risk of obesity and T2D onset associated to ageing. On the other hand, obesity and T2D, the paradigms of AT dysfunction, share many physiological characteristics with the ageing process, such as an increased burden of senescent cells and epigenetic alterations. Thus, these chronic metabolic disorders may represent a state of accelerated ageing. MATERIALS AND

methodsA more precise explanation of the fundamental ageing mechanisms that occur in AT and a deeper understanding of their role in the interplay between accelerated ageing and AT dysfunction can be a fundamental leap towards novel therapies that address the causes, not just the symptoms, of obesity and T2D, utilizing strategies that target either senescent cells or DNA methylation.

resultsIn this review, we summarize the current knowledge of the pathways that lead to AT dysfunction in the chronological ageing process as well as the pathophysiology of obesity and T2D, emphasizing the critical role of cellular senescence and DNA methylation.

conclusionFinally, we highlight the need for further research focused on targeting these mechanisms.

Indexed as

Metabolic DiseasesAdipose TissueAgedAged, 80 and overAgingCellular SenescenceChronic DiseaseDNA MethylationHumansMiddle AgedSignal TransductionAdipose tissueAgeingCellular senescenceDNA methylationObesityType 2 diabetes

Identifiers

PMID32358737
PMCPMC7481162
OpenAlexW3022432727

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.