ReviewFrontiers in cardiovascular medicine2022
Targeting GPCRs to treat cardiac fibrosis.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- TFAP4 exacerbates pathological cardiac fibrosis by modulating mechanotransduction.Cell insight · 2025Article
- Fibrosis: cross-organ biology and pathways to development of innovative drugs.Nature reviews. Drug discovery · 2025Review
- Imaging methods to monitor and quantify cell differentiation.Frontiers in cell and developmental biology · 2025Review
- Fibroblast and myofibroblast activation in normal tissue repair and fibrosis.Nature reviews. Molecular cell biology · 2024Review
- Cellular reprogramming of fibroblasts in heart regeneration.Journal of molecular and cellular cardiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis occurs ubiquitously in ischemic heart failure, genetic cardiomyopathies, diabetes mellitus, and aging. It triggers myocardial stiffness, which impairs cardiac function, ultimately progressing to end-stage heart failure and increased mortality. Although several targets for anti-fibrotic therapies have been identified, including TGF-β and receptor tyrosine kinase, there is currently no FDA-approved drug specifically targeting cardiac fibrosis. G protein-coupled receptors (GPCRs) are integral, multipass membrane-bound receptors that exhibit diverse and cell-specific expression, offering novel and unrealized therapeutic targets for cardiac fibrosis. This review highlights the emerging roles of several GPCRs and briefly explores their downstream pathways that are crucial in cardiac fibrosis. We will not only provide an overview of the GPCRs expressed on cardiac fibroblasts that are directly involved in myofibroblast activation but also describe those GPCRs which contribute to cardiac fibrosis via indirect crosstalk mechanisms. We also discuss the challenges of identifying novel effective therapies for cardiac fibrosis and offer strategies to circumvent these challenges.
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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.