Evidence mapPaperPMID 41450977Full record

ArticleActa biochimica Polonica2025

Gasocrine hypothesis - a potential supplement to cell theory.

Savani Anbalagan

Abstract read
In one paragraph

Article in Acta biochimica Polonica, 2025. 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

1 author.

Savani AnbalaganInstitute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznań, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Biology textbooks lack precise terms to describe oxygen-based inter-organismal signaling between oxygen-producing and aerobic organisms. To address this gap, I recently proposed the concept of gasocrine signaling, which encompasses all signaling mediated by gaseous molecules and gasoreceptors within and between cells, organisms, and even abiotic factors. Given the fundamental importance of gaseous molecules for life, I propose the gasocrine hypothesis: all cells require gasocrine signaling. This hypothesis can be divided into three sub-hypotheses: First, all living organisms composed of one or more cells require gasocrine signaling to sense, communicate, grow, and propagate. Second, gasocrine signaling mediated via gasoreceptor proteins (or yet to be identified gas-sensing riboceptors) is the most essential cellular and inter-organismal signaling. Third, acellular entities arising from or replicating in pre-existing cells require gasocrine signaling. I propose several potential experiments to falsify these hypotheses. If they withstand falsification, the gasocrine hypothesis would supplement cell theory. It would also provide a novel framework for understanding fundamental biological principles, cellular and organismal communication, and the role of abiotic factors. Furthermore, it establishes the foundation for the emerging field of gasocrinology, which is critical in the context of a changing environment.

Indexed as

GasesModels, BiologicalOxygenSignal TransductionAnimalsHumansGasesOxygencell theorygaseous signaling moleculegasocrine signalinggasocrinologygasoreceptorgas sensingquorum sensingriboceptor

Identifiers

PMID41450977
PMCPMC12732322

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.