Article in American journal of physiology. Heart and circulatory physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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.
Gaurav SarodeDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.
Daphne Agostina DilorettoDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.ORCID 0000-0002-2386-2119
Fatin Fazrina RoslanDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.
Prisha PanditaDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.
James OvertonDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.
Uma SrivatsaDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.
Jorge Manuel CatripDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.ORCID 0000-0001-5849-2819
David A LiemDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.ORCID 0009-0001-5796-309X
Heejung BangAHA Strategically Focused Research Network to study Chronic Psychosocial Stressors, Sacramento, California, United States.
Martin CadeirasDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.ORCID 0000-0003-4545-2871
Nipavan ChiamvimonvatDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.
Padmini SirishDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California, United States.ORCID 0000-0002-9216-279X
Funding
Functional Interactions of Cardiac Ion ChannelsR01HL085844 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2007 to 2025
$7.3M
Training Program In Basic & Translational Cardiovascular ScienceT32HL086350 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, David A. Liem · 2008 to 2026
$7.1M
Translational Study of Cardiac DysfunctionR01HL085727 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN, SIRISH, PADMINI · 2008 to 2022
$5.7M
Initiative for Maximizing Student Development at the University of California, Davis.T32GM135741 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ALDRIN V. GOMES, Manuel F Navedo · 2020 to 2026
$3.2M
A prospective multiethnic HFpEF cohort from Californias Central ValleyU01HL160274 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, Nipavan Chiamvimonvat · 2021 to 2026
$2.3M
Decoding the enigma of cardiac amplificationR01HL137228 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2017 to 2020
$2.2M
Molecular Mechanisms of Atrial Fibrillation: A Multimodal AnalysisR01HL170520 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Nipavan Chiamvimonvat, Vladimir Filkov · 2024 to 2026
$1.8M
FUNCTIONAL PROPERTIES OF CA PUMPS IN HAIR CELLR01DC004215 · NIDCD · UNIVERSITY OF CINCINNATI · PI YAMOAH, EBENEZER N. · 1999 to 2003
$1.0M
Cardiac Regenerative Therapy Using Gene-Edited Stem Cells to Improve Transplantation OutcomesR56HL167932 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SIRISH, PADMINI · 2023 to 2023
$400k
Mechanisms Underpinning Afterload-Induced Atrial FibrillationF31HL168956 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DILORETTO, DAPHNE AGOSTINA · 2023 to 2024
$81k
American Heart Association (AHA) 18CDA3411006American Heart Association (AHA) 23SFRNCCS1052478American Heart Association (AHA) 23SFRNPCS1060482BLRD VA I01 BX000576CSRD VA I01 CX001490Health Resources in Action (HRiA) Harold S. Geneen Trust AwardHHS | National Institutes of Health (NIH) F31HL168956HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL085727HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL170520HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) U01HL160274HHS | NIH | NHLBI | Division of Intramural Research (DIR) R56HL167932NHLBI NIH HHS F31 HL168956NHLBI NIH HHS R01 HL085727NHLBI NIH HHS R01 HL085844NHLBI NIH HHS R01 HL137228NHLBI NIH HHS R01 HL170520NHLBI NIH HHS R56 HL167932NHLBI NIH HHS T32 HL086350NHLBI NIH HHS U01 HL160274NIDCD NIH HHS R01 DC004215NIGMS NIH HHS T32 GM135741Rosenfeld Family Foundation Rosenfeld AwardTobacco-Related Disease Research Program (TRDRP) T32KT4729UC | University of California, Davis (UCD) Internal Medicine Chair's Research Award
6 · The paper itself
Abstract
Atrial fibrillation (AF) represents one of the most common arrhythmias seen clinically and is associated with a significant increase in morbidity and mortality. One of the main contributors to the pathophysiology for the initiation, progression, and persistence of AF is inflammation. Inflammatory infiltrates and increased serum levels of proinflammatory cytokines have been demonstrated in animal models and patients with AF. AF progression is associated with increased levels of these proinflammatory cytokines. Cigarette smoking is associated with an increased risk of AF. Moreover, cigarette smoke is known to increase inflammation and proinflammatory cytokines including interleukin (IL)-1β, IL-18, and tumor necrosis factor-α (TNF-α). Therefore, it is of great clinical importance to elucidate the underlying mechanisms contributing to smoking-induced inflammation in patients with AF. A critical amplifier of inflammation is the NLRP3 inflammasome, which is increased in patients with AF. Here, we identify critical upstream mechanisms leading to NLRP3 inflammasome activation via endoplasmic reticulum stress in atrial tissues from patients with AF and human-induced pluripotent stem cell-atrial cardiomyocytes. These findings reveal important mechanistic insights into possible upstream targets in controlling excessive inflammation due to smoking in patients with AF.
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.
Cigarette smoking induces NLRP3 inflammasome activation in patients with atrial fibrillation. · full record | Socratic