Key result
Elevated Galectin-3 linked to ~2.6-fold higher risk of major cardiovascular events and hospitalization in dilated cardiomyopathy.
Why the study?
Previous reviews of myocardial fibrosis in dilated cardiomyopathy focused on individual fibrosis markers or static histological assessments, leaving mechanistic and clinical uncertainties around the complementary roles and combined prognostic value of Galectin-3 and PIIINP.
Does the combined detection of Galectin-3 and PIIINP improve risk stratification and prediction of major adverse cardiovascular events in patients with dilated cardiomyopathy?
Does the combined detection of Galectin-3 and PIIINP improve risk stratification and prediction of major adverse cardiovascular events in patients with dilated cardiomyopathy?
Answers are grounded in this paper and cite their sources.
Combining Galectin-3 (an upstream inflammatory-fibrotic trigger) and PIIINP (a downstream marker and effector of active type III collagen synthesis) provides complementary prognostic value for predicting major adverse cardiovascular events and guiding anti-fibrotic therapy in dilated cardiomyopathy.
Dilated cardiomyopathy (DCM) is characterized by ventricular dilation and systolic dysfunction, and the associated pathophysiology is closely linked to myocardial fibrosis, a key contributor to disease progression and poor prognosis. Galectin-3 (Gal-3) plays a crucial role in initiating early proinflammatory and profibrotic signaling. Meanwhile, type III procollagen N-terminal propeptide (PIIINP) serves as a marker of type III collagen synthesis and acts as an active profibrotic effector. The counterpart to PIIINP, type III procollagen C-terminal propeptide (PIIICP), is released during type III collagen maturation, reflecting distinct processing and clearance dynamics. PIIINP promotes fibrosis through integrin α2β1/discoidin domain receptor 1 (DDR1)-mediated extracellular signal-regulated kinase (ERK)/phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling and contributes to the establishment of a Gal-3-transforming growth factor-β (TGF-β)-PIIINP positive feedback loop, thereby linking inflammation to extracellular matrix deposition. Recently, Gal-3 and PIIINP have gained recognition as valuable biomarkers for the diagnosis, risk stratification, and prognosis assessment of DCM. Unlike previous reviews that focused solely on individual fibrosis markers or static histological assessments, this review uniquely highlights the complementary roles of Gal-3 and PIIINP. These markers are crucial for understanding inflammatory-fibrotic activation and dynamic collagen turnover. This review systematically outlines the expression patterns of these markers across various stages of DCM and underscores the additional prognostic value of the associated combined detection beyond traditional indicators. Among the components of major adverse cardiovascular events (MACE), heart failure hospitalization and cardiovascular mortality are most strongly associated with elevated levels of Gal-3 and PIIINP in patients with DCM. Specifically, Gal-3 levels of ≥14.54 ng/mL are closely linked to increased risks of heart failure readmission and sudden cardiac death. In contrast, elevated PIIINP levels are most strongly associated with heart failure hospitalization and ventricular arrhythmias. This review aims to elucidate the specific biological functions of Gal-3 and PIIINP, address both mechanistic and clinical uncertainties, and summarize evidence-based thresholds for risk stratification. This review also seeks to provide theoretical insights and clinical guidance for early intervention and personalized anti-fibrotic therapy in DCM. A systematic search was conducted in PubMed, Embase, and Web of Science, covering literature from inception to March 2026. The search used keywords such as "dilated cardiomyopathy", "myocardial fibrosis", "Galectin-3", "PIIINP", "biomarker", and "cardiovascular events". The review included studies comprising clinical trials, observational research, and mechanistic investigations of Gal-3 and PIIINP in DCM. Reviews, case reports, and non-English literature were excluded. Data were synthesized using a narrative review approach.
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Zhao et al. (2026) conducted a review in Dilated cardiomyopathy (DCM) and myocardial fibrosis. Elevated Galectin-3 (≥14.54 ng/mL) and PIIINP (≥97 ng/mL) levels vs. Lower biomarker levels (Gal-3 <14.54 ng/mL, PIIINP <97 ng/mL) was evaluated on Major adverse cardiovascular events (MACE), including heart failure hospitalization, cardiovascular mortality, and ventricular arrhythmias. Galectin-3 levels ≥14.54 ng/mL confer a 2.6-fold higher risk of emergency hospitalization and major cardiovascular events in dilated cardiomyopathy, with PIIINP adding complementary prognostic value.
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