eScholarship
metadata only
CC BY
Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias
Millions of people suffer a myocardial infarction (MI) every year, and those who survive have increased risk of arrhythmias and sudden cardiac death. Recent clinical studies have identified sympathetic denervation as a predictor of increased arrhythmia susceptibility. Chondroitin sulfate proteoglyca
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- Protein tyrosine phosphatase 1B (PTP1B) as a potential therapeutic target for neurological disorders#948155
- The Role of Pioglitazone in Vascular Transcriptional Remodeling#1010222
- Modulation of Fibrosis-inducing Pathways in Acute Myocardial Infarction#870749
- Early Mineralocorticoid Receptor Antagonist Treatment to Reduce Myocardial Infarct Size#865760
- CaMKIIα holoenzymes self-organize into chain-like mesoscale clusters#784468
Record · ID 1440844
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive