Evidence map›Paper›PMID 41557238›Full record

ReviewSub-cellular biochemistry2026

The Impact of Ageing on Fibrillar Collagens.

Elizabeth G Canty-Laird, Himadri S Gupta, Helen L Birch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Sub-cellular biochemistry, 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

3 authors.

Elizabeth G Canty-LairdDepartment of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, William Henry Duncan Building, Liverpool, UK. elizabeth.laird@liverpool.ac.uk.
Himadri S GuptaSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Helen L BirchUniversity College London, Stanmore Campus, Brockley Hill, Stanmore, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The world population is ageing rapidly. The over-60s now outnumber the under- 5s, and 1 in 6 people will be over 60 by 2030 (WHO). Collagen is a key structural component of many tissues and organs, and although a fraction of the collagenous component of tissues is remarkably long-lived, it progressively accumulates damage over a lifetime. The capacity for new collagen synthesis and post-translational modification is altered and dysregulated during ageing. The mature crosslinks that stabilise collagenous tissues can remain stable or increase with age, whereas age-related glycation end-products can increase and affect tissue biomechanics. At the fibrillar nanoscale, changes associated with ageing and disease influence fibril deformation and stress transfer in a tissue-specific manner. Age-related loss of collagen can be caused by proteolytic degradation, but normal collagen turnover is also affected by ageing and its dysregulation is detrimental to tissue homeostasis. Age-related accumulation of senescent cells may contribute to the aberrant turnover of collagen during ageing. Finally, collagen itself may hold the key to counteracting some of the detrimental effects of ageing, with ingested hydrolysed collagen peptides demonstrating beneficial effects on skin and the musculoskeletal system.

Indexed as

AgingFibrillar CollagensAnimalsGlycation End Products, AdvancedHumansProtein Processing, Post-TranslationalProteolysisFibrillar CollagensGlycation End Products, AdvancedAgeingCollagenCrosslinkingDegradationNanomechanicsNanostructureSenescenceSupplementsTurnover

Identifiers

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.