ReviewFrontiers in pharmacology2026
Immune checkpoint inhibitor-related cardiotoxicity: a cellular pharmacology perspective on susceptibility and resistance.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune checkpoint inhibitors (ICIs) have reshaped the treatment landscape of cancer, yet their clinical benefit is accompanied by a distinct spectrum of immune-related toxicities. Among these, cardiotoxicity remains uncommon but clinically consequential because it can evolve quickly, presents with marked heterogeneity, and may result in fulminant myocarditis, malignant arrhythmia, or hemodynamic collapse. Key mechanistic drivers include T-cell clonality directed against cardiac autoantigens (e.g., α-myosin heavy chain), cytokine amplification via JAK/STAT signaling, and innate immune recruitment. Recent work has shifted the field away from viewing ICI-related cardiotoxicity as a nonspecific inflammatory complication. Instead, available data support a model in which immune checkpoint blockade perturbs a broader tumor-host ecosystem and exposes organ-specific vulnerabilities within the heart. T-cell clonality, loss of peripheral tolerance, cytokine amplification, endothelial activation, stromal remodeling, and metabolic rewiring all appear to contribute, although their relative importance likely varies across patients. This review examines ICI-associated cardiotoxicity through the lens of cellular pharmacology. We focus on how checkpoint signaling sustains cardiac immune homeostasis, how susceptibility emerges from interactions between tumor-derived cues and host immune context, and why resistance to toxicity-directed therapy remains clinically relevant. We also discuss evolving biomarker strategies-including high-sensitivity troponins, cardiac MRI, and emerging immune-state markers-and mechanism-based interventions that may help reduce cardiac injury without fully negating antitumor efficacy. By framing cardiotoxicity as a context-dependent extension of systemic immune modulation rather than an isolated adverse event, we highlight unresolved questions that are central to the development of predictive biomarkers and more selective therapeutic strategies. Finally, we briefly note that structured nursing surveillance and multidisciplinary team coordination remain essential for translating mechanistic advances into improved bedside outcomes.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.