Evidence map›Paper›PMID 37250776›Full record

ReviewiScience2023

Accelerating aging with dynamic biomaterials: Recapitulating aged tissue phenotypes in engineered platforms.

Christopher M Madl

Abstract readReview
In one paragraph

Review in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
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

1 author.

Christopher M MadlDepartment of Materials Science and Engineering, School of Engineering and Applied Sciences, University of Pennsylvania, Philadelphia, PA 19104, USA.

Funding

Elucidating Effects of Fibrosis on Aged Stem Cells with Dynamic BiomaterialsR00AG071738 · NIA · UNIVERSITY OF PENNSYLVANIA · PI MADL, CHRISTOPHER MATTHEW · 2023 to 2025
$742k
NIA NIH HHS R00 AG071738
6 · The paper itself

Abstract

Aging is characterized by progressive decline in tissue function and represents the greatest risk factor for many diseases. Nevertheless, many fundamental mechanisms driving human aging remain poorly understood. Aging studies using model organisms are often limited in their applicability to humans. Mechanistic studies of human aging rely on relatively simple cell culture models that fail to replicate mature tissue function, making them poor surrogates for aged tissues. These culture systems generally lack well-controlled cellular microenvironments that capture the changes in tissue mechanics and microstructure that occur during aging. Biomaterial platforms presenting dynamic, physiologically relevant mechanical, structural, and biochemical cues can capture the complex changes in the cellular microenvironment in a well-defined manner, accelerating the process of cellular aging in model laboratory systems. By enabling selective tuning of relevant microenvironmental parameters, these biomaterials systems may enable identification of new therapeutic approaches to slow or reverse the detrimental effects of aging.

Indexed as

BioengineeringBiomaterialsHealth sciences

Identifiers

PMID37250776
PMCPMC10213044

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.