sST2 in the Literature: A Starting Reading List

Updated 2026-09-28

A short reading list for groups entering sST2 work — and why we publish a reading list rather than a citation count.

Why a reading list, not a citation count

Several suppliers display the number of papers citing their own catalogue numbers. That is a genuine signal — but it is their number, built over decades, and we have no honest claim to it. What we can usefully offer is the literature on the analyte itself, so a new group can get oriented quickly.

Foundational biology

Weinberg et al., Circulation 2002 — expression and regulation of ST2 in cardiomyocytes and myocardial infarction. Sanada et al., Journal of Clinical Investigation 2007 — IL-33 and ST2 as a biomechanically induced, cardioprotective signalling system. Together these established why the soluble receptor is worth measuring at all.

Clinical and consensus literature

Januzzi et al., Journal of the American College of Cardiology 2007 — measurement of the interleukin family member ST2 in patients with acute dyspnoea. Pascual-Figal and Januzzi, American Journal of Cardiology 2015 — the biology of ST2, from the International ST2 Consensus Panel. If you are setting up an sST2 assay for the first time, start with the consensus paper.

How to use this list

These references concern the analyte and its biology, not our materials — we cite them to save you a literature search, and you should verify details against the original publications — searching the title in PubMed is the fastest route. We give author, journal and year rather than publisher links, because publisher URLs change and a dead link is worse than no link. If you are deciding between measuring soluble ST2 and a natriuretic peptide, the consensus paper and our comparison article answer that from different directions.

How to read the clinical literature critically

Two habits help when working through this literature. The first is to distinguish mechanism papers from prognostic studies from consensus documents, because they carry different weight and answer different questions: the first two in this list established that the soluble receptor is regulated in the heart and that the IL-33/ST2 system is biomechanically induced and cardioprotective, while the clinical studies that followed measured whether the marker carries information. The second is to notice the cut-off. Prognostic studies of sST2 report a variety of decision thresholds, and a threshold derived in one cohort does not necessarily transport to another with a different case mix, assay and sample-handling protocol. A pooled analysis across cohorts is a stronger basis for a general claim about prognosis than any single-centre result, and it also makes the heterogeneity between studies visible instead of hiding it.

From literature to specification

Reading the literature is not only about the biology; it tells you what your reagent has to survive. Serial measurement, which the prognostic studies depend on, converts lot consistency from a convenience into a requirement, because a shift between lots can look exactly like a change in the patient. Studies that report the marker alongside a natriuretic peptide imply that both analytes have to behave comparably in the same sample matrix, which constrains buffer and diluent choices for both assays rather than one. And the consensus literature makes explicit that the marker is interpreted in a clinical context rather than as a stand-alone result — a reminder that if you are building an assay, the analytical performance that matters is the performance near the decision threshold you intend to use, not the limit of detection on a specification sheet.

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