Introduction
Dapagliflozin, a pioneering SGLT2 inhibitor, has evolved from a diabetes medication to a cornerstone therapy for heart failure (HF). Built on pivotal trials such as DAPA-HF and DELIVER, its role now spans reduced and preserved ejection fraction HF subtypes, with ongoing investigations into cardiorenal protection and fibrosis modulation. This article interprets a comprehensive bibliometric analysis of dapagliflozin research in HF from 2012 to 2024, revealing publication trends, collaborations, and emerging scientific themes to guide future work.
Publication Trends and Global Leadership
Analyzing 919 publications across 76 countries/regions shows a clear upward trajectory since 2016, with a notable acceleration after 2019—the year of the landmark DAPA-HF trial. The United States leads in publication output, followed closely by Sweden and China. While US-led activity reflects strong clinical and translational contributions, the landscape is becoming increasingly international, underscoring growing global interest in SGLT2 inhibitors for HF.
Key Contributors
Among individual authors, Anna Maria Langkilde, Mikhail N. Kosiborod, and Scott D. Solomon are the most prolific. Yet, a notable insight from centrality metrics is that prolific authors often operate in relatively insular collaboration clusters; bridging roles are exemplified by researchers like McMurray John J V, who connects disparate groups. This pattern highlights a structural gap: opportunities to foster broader, more integrated collaboration networks.
Institutional and Country Networks
Top institutions driving the dapagliflozin HF literature include AstraZeneca, Harvard University, and Brigham and Women’s Hospital. AstraZeneca stands out as a central knowledge broker, while academic centers across the United States, Europe, and Asia contribute substantial volumes. The country network reveals a similar theme: the United States, Sweden, and China publish the most, with relatively low betweenness centrality values. This suggests geopolitical silos that could restrict cross-pollination of ideas and clinical practice insights.
Hotspots: What the Field Is Moving Toward
Keyword analyses cluster around several core themes: disease subtypes (HF with reduced ejection fraction and preserved ejection fraction), cardiorenal outcomes, combination therapies, and underlying mechanisms (inflammation, fibrosis, and oxidative stress). Dapagliflozin’s expanding scope includes renal protection and its integration with other therapies such as mineralocorticoid receptor antagonists (MRAs). Notably, “reduced ejection fraction” and “preserved ejection fraction” are phenotypes receiving heightened attention, signaling a shift from HFpEF neglect to more robust, targeted investigations.
Clinical Outcomes and Mechanisms
Evidence from major trials underscores reductions in cardiovascular death and HF hospitalizations, with benefits observed irrespective of diabetes status. The field increasingly links improved outcomes to mechanisms such as anti-fibrotic effects, attenuation of inflammation, and mitigation of oxidative stress. Mechanistic research explores pathways like AMPKα and TGF-β/Smad signaling, EndMT, and the Nrf2 axis, reflecting a move toward translating basic science into predictive clinical impact.
Therapeutic Strategies and Future Directions
Bibliometric patterns point to two pragmatic frontiers. First, combining dapagliflozin with novel non-steroidal MRAs is a prime area of interest for HF management, especially in HFpEF where therapeutic options are limited. Second, the synergy of dapagliflozin with other guideline-directed therapies—renin–angiotensin system inhibitors, beta-blockers, and MRAs—continues to mature into “quadruple therapy” for HF. Beyond cardiology, attention to kidney outcomes, albuminuria, and renal protection remains integral due to the intertwined cardiorenal biology of HF.
Limitations and Takeaways for Researchers
Bibliometric studies rely on databases like Web of Science and analytic tools that detect publication patterns but cannot replace randomized trials. Language bias and evolving indexing can influence results. Nevertheless, the analysis identifies clear gaps: a need for broader international collaboration networks, deeper mechanistic studies of anti-fibrotic effects, and expanded HFpEF research. By bridging collaborations and prioritizing integrated, phenotype-tailored trials, the field can better define dapagliflozin’s role across HF spectrums.
Conclusion
From 2012 to 2024, dapagliflozin’s journey in HF research reflects a field converging on cardiorenal protection, mechanism-driven insights, and inclusive trials across HF subtypes. The next era likely features intensified HFpEF investigations, innovative combination therapies, and a more interconnected global research community—driving toward optimized, evidence-based care for patients with heart failure.
