Evidence map›Paper›PMID 42051247›Full record

ReviewFrontiers in clinical diabetes and healthcare2026

The role of chromogranin A cleavage products in onset of type 1 and 2 diabetes.

Gustaf Christoffersson, Elke M Muntjewerff

Abstract readReview
In one paragraph

Review in Frontiers in clinical diabetes and healthcare, 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

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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

2 authors.

Gustaf Christoffersson *Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Elke M Muntjewerff *Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromogranin A (CgA) is a pro-hormone widely expressed in neuroendocrine tissues and elevated in both type 1 (T1D) and type 2 diabetes (T2D). Its diverse biological effects arise from proteolytic cleavage into six bioactive peptides: vasostatin I and II (VS-I/II), chromofungin (CHR), pancreastatin (PST), catestatin (CST), WE-14, and serpinin-each exerting distinct and sometimes opposing functions. This review covers current knowledge on the activity, circulating levels, and mechanistic roles of these peptides in diabetes pathogenesis and progression. Evidence indicates contrasting peptide profiles in T1D and T2D: PST levels are elevated in T2D and promote inflammation, gluconeogenesis, and insulin resistance, whereas CST levels are reduced and exert anti-inflammatory and insulin-sensitizing effects. In T1D, CST and VS-I are increased early after diagnosis, with VS-I and WE-14 functioning as autoantigens that drive autoreactive T cell responses. Knockout mouse models further demonstrate that loss of CgA or CST profoundly alters glucose homeostasis, macrophage polarization, catecholamine release, and diabetes susceptibility. Emerging data highlight a complex nerve-immune-endocrine axis through which CgA peptides regulate metabolic and inflammatory pathways. Collectively, CgA-derived peptides represent promising biomarkers and therapeutic targets, though further translational studies remain essential to define their diagnostic and clinical potential.

Indexed as

catestatinchromogranin Adiabetes type 1diabetes type 2pancreastatinserpininvasostatinWE14

Identifiers

PMID42051247
PMCPMC13110968

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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.