ArticleCell proliferation2025
Primary Cilia Orchestrate Cardiac Pathogenesis: A Central Nexus of Remodeling, Signaling, and Repair.
Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Tubulin Post-Translational Modifications in Cardiovascular Diseases: Emerging Mechanisms and Therapeutic Modulation by Traditional Chinese Medicine.Drug design, development and therapy · 2026Review
- Primary Cilia Orchestrate Cardiac Pathogenesis: A Central Nexus of Remodeling, Signaling, and Repair.Cell proliferation · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Roles of primary cilia and the signals they transmit in the development of myocardial fibrogenesis, cardiac hypertrophy, and atrial fibrillation. Left, Fibroblasts can differentiate into myofibroblasts in response to TGF-β1. TGF-β1 stimulation via both paracrine action in the heart and exogenous action on primary cultured fibroblasts activated the phosphorylation of SMAD3 and the transcription of the fibronectin and collagen type I and III genes. Middle, Vesicles derived from cilia are secreted at an accelerated rate under fluid shear stress. Blockage of ciliary protein, which is required for cELV generation with shRNA, led to blunted cELV secretion and left ventricular hypertrophy. Right, under pathological conditions such as atrial fibrillation (AF), fibroblasts exhibit increased proliferation and differentiation into α-smooth muscle Actin (αSMA)-expressing myofibroblasts. This disrupts ECM dynamics, ultimately leading to interstitial fibrosis within the atria. AF patients presented increased HDAC6 activity and reduced levels of acetylated α-tubulin in left atrial tissues. HDAC6 activity is activated by the interaction of aurora kinase A (AURKA), and neural precursor cells express developmentally downregulated protein 9 (NEDD9) via phosphorylation. LiCl prompts the reversion of αSMA-positive myofibroblasts into αSMA-negative fibroblasts.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.