Review in Physiology (Bethesda, Md.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing 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.
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.
Cameron R RostronDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, United States.ORCID 0000-0003-4727-3420
Carmella Evans-MolinaDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States.ORCID 0000-0001-7764-8663
Funding
Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Carmella Evans-Molina · 2015 to 2026
$17.4M
The Integrated Stress Response in Human Islets During Early T1DU01DK127786 · NIDDK · UNIVERSITY OF CHICAGO · PI EVANS-MOLINA, CARMELLA, MIRMIRA, RAGHAVENDRA G · 2020 to 2025
$7.1M
RESEARCH TRAINING PROGRAM IN DIABETES AND OBESITYT32DK064466 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Carmella Evans-Molina, RONALD C WEK · 2003 to 2026
$5.2M
Mechanisms of Beta Cell Function in Health and DiseaseR01DK093954 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA · 2011 to 2019
$3.5M
Implications of Changes in Islet Exosomal Cargo in Type 1 DiabetesR01DK133881 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA, MIRMIRA, RAGHAVENDRA G · 2022 to 2025
$2.7M
Biomarkers Of Beta Cell Stress In Type 1 Diabetes (BetaMarker)UC4DK104166 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EIZIRIK, DECIO LAKS, EVANS-MOLINA, CARMELLA · 2014 to 2014
$2.4M
Indiana University clinical Center for acute pancreatitis and diabetes clinical research networkU01DK127382 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Carmella Evans-Molina, Evan L Fogel · 2020 to 2026
$2.4M
Control of beta cell function and survival by RYR2-mediated calcium signalsR01DK127236 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA · 2021 to 2025
$2.2M
β cell miRNAs Function as Molecular Hubs of Type 1 Diabetes PathogenesisR01DK127308 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA · 2021 to 2024
$1.7M
BLRD VA I01 BX001733Breakthrough T1DHHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) 5T32DK064466-22HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) P30-DK-097512HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01DK093954HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01DK127236HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01DK127308HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) U01DK127786HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) UC4DK104166Leona M. and Harry B. Helmsley Charitable Trust (Helmsley Charitable Trust)NIDDK NIH HHS P30 DK097512NIDDK NIH HHS R01 DK093954NIDDK NIH HHS R01 DK127236NIDDK NIH HHS R01 DK127308NIDDK NIH HHS R01 DK133881NIDDK NIH HHS T32 DK064466NIDDK NIH HHS U01 DK127382NIDDK NIH HHS U01 DK127786NIDDK NIH HHS UC4 DK104166U.S. Department of Veterans Affairs (VA) I01BX001733
6 · The paper itself
Abstract
Type 1 diabetes (T1D) is a metabolic disease caused by the autoimmune-mediated destruction of pancreatic β-cells; however, recent findings indicate that intrinsic stress pathways within β-cells may contribute to the initiation or perpetuation of autoimmunity. Here, we discuss the molecular and inflammatory etiologies of β-cell dysfunction in T1D, with a focus on cytokine signaling, endoplasmic reticulum stress, mitochondrial dysfunction, and senescence.
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.
Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes. · full record | OpenQuestion