Evidence map›Paper›PMID 37216041›Full record

ArticleFrontiers in network physiology2023

Dynamic model assuming mutually inhibitory biomarkers of frailty suggests bistability with contrasting mobility phenotypes.

Nathan Schaumburger, Joel Pally, Ion I Moraru, Jatupol Kositsawat, George A Kuchel, Michael L Blinov

Open access · goldAbstract read
In one paragraph

Article in Frontiers in network physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

6 authors at 1 institution in 1 country.

Nathan SchaumburgerDepartment of Ecology and Evolutionary Biology, University of Connecticut, Storrs, CT, United States.
Joel PallyCenter for Cell Analysis and Modeling, UConn Health, Farmington, CT, United States.
Ion I MoraruCenter for Cell Analysis and Modeling, UConn Health, Farmington, CT, United States.
Jatupol KositsawatUConn Center on Aging, UConn Health, Farmington, CT, United States.
George A KuchelUConn Center on Aging, UConn Health, Farmington, CT, United States.
Michael L BlinovCenter for Cell Analysis and Modeling, UConn Health, Farmington, CT, United States.
UConn Health · US

Funding

Mechanistic Modeling of Cellular SystemsR24GM137787 · NIGMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI Pedro Mendes, Ion I. Moraru · 2020 to 2026
$8.9M
NIGMS NIH HHS R24 GM137787
6 · The paper itself

Abstract

Bistability is a fundamental biological phenomenon associated with "switch-like" behavior reflecting the capacity of a system to exist in either of two stable states. It plays a role in gene regulation, cell fate switch, signal transduction and cell oscillation, with relevance for cognition, hearing, vision, sleep, gait and voiding. Here we consider a potential role for bistability in the existence of specific frailty states or phenotypes as part of disablement pathways. We use mathematical modeling with two frailty biomarkers (insulin growth factor-1, IGF-1 and interleukin-6, IL-6), which mutually inhibit each other. In our model, we demonstrate that small variations around critical IGF-1 or IL-6 blood levels lead to strikingly different mobility outcomes. We employ deterministic modeling of mobility outcomes, calculating the average trends in population health. Our model predicts the bistability of clinical outcomes: the deterministically-computed likelihood of an individual remaining mobile, becoming less mobile, or dying over time either increases to almost 100% or decreases to almost zero. Contrary to statistical models that attempt to estimate the likelihood of final outcomes based on probabilities and correlations, our model predicts functional outcomes over time based on specific hypothesized molecular mechanisms. Instead of estimating probabilities based on stochastic distributions and arbitrary priors, we deterministically simulate model outcomes over a wide range of physiological parameter values within experimentally derived boundaries. Our study is "a proof of principle" as it is based on a major assumption about mutual inhibition of pathways that is oversimplified. However, by making such an assumption, interesting effects can be described qualitatively. As our understanding of molecular mechanisms involved in aging deepens, we believe that such modeling will not only lead to more accurate predictions, but also help move the field from using mostly studies of associations to mechanistically guided approaches.

Indexed as

agingbistabiitydynamical modelfrailtyIGF-1IL-6mathematical modelphenotype

Identifiers

PMID37216041
PMCPMC10192762
OpenAlexW4368367933

What OpenQuestion 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 OpenQuestion graph.