ArticleDiabetes2024
Bidirectional Mendelian Randomization Highlights Causal Relationships Between Circulating INHBC and Multiple Cardiometabolic Diseases and Traits.
Article in Diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
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Who cites it
7 citing papers in PubMed.
- Paediatric proteomic signatures of cardiometabolic disease-associated traits predict adult disease outcomes.Nature metabolism · 2026Article
- Circulating proteins altered in response to the Dietary Approaches to Stop Hypertension (DASH) diet suggest underlying molecular mechanisms and long-term health benefits.medRxiv : the preprint server for health sciences · 2026Article
- Proteogenomic Analysis of Coronary Artery Calcification in Human Populations.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- A Mendelian randomization-based drug repurposing pipeline: application to lipid traits and coronary artery disease.medRxiv : the preprint server for health sciences · 2026Article
- Genetic associations of circulating plasma proteins with cardiometabolic diseases.Genome biology · 2026Article
- Association Between Waist Circumference and Coronary Artery Disease: Evidence from the NHANES 1999-2023 Cross-Sectional Data and Mendelian Randomization Analysis.Global heart · 2026Article
- Activin Actions in Adipocytes.The Journal of clinical endocrinology and metabolism · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Human genetic and transgenic mouse studies have highlighted a potential liver-adipose tissue endocrine axis, involving activin C (Act-C) and/or Act-E and ALK7, influencing fat distribution and systemic metabolism. We investigated the bidirectional effects between circulating INHBC, which homodimerizes into Act-C, and adiposity traits, insulin resistance, inflammation, and cardiometabolic disease risk. Additionally, we examined whether Act-C is an ALK7 ligand in human adipocytes. We used Mendelian randomization and in vitro studies in immortalized human abdominal and gluteal adipocytes. Circulating INHBC was causally linked to reduced lower-body fat, dyslipidemia, and increased risks of coronary artery disease (CAD) and nonalcoholic fatty liver disease (NAFLD). Conversely, upper-body fat distribution, obesity, hypertriglyceridemia, subclinical inflammation, and type 2 diabetes positively impacted plasma INHBC levels. Mechanistically, an atherogenic lipid profile may partly explain the INHBC-CAD link, while inflammation and hypertriglyceridemia may partly explain how adiposity traits affect circulating INHBC. Phenome-wide Mendelian randomization showed weak causal relationships between higher plasma INHBC and impaired kidney function and higher gout risk. In human adipocytes, recombinant Act-C activated SMAD2/3 signaling via ALK7 and suppressed lipolysis. In summary, INHBC influences systemic metabolism by activating ALK7 in adipose tissue and may serve as a drug target for atherogenic dyslipidemia, CAD, and NAFLD. ARTICLE HIGHLIGHTS:
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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.