ReviewReviews in cardiovascular medicine2026
Chronic Inflammation and Coronary Microvascular Dysfunction.
Review in Reviews in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
5 authors.
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Abstract
Coronary microvascular dysfunction (CMD) represents a pivotal pathological hallmark across diverse cardiovascular pathologies, the progression of which is tightly coupled to systemic chronic inflammation. Clinically, CMD presents as ischemia with non-obstructive coronary arteries (INOCAs) and myocardial infarction with non-obstructive coronary arteries (MINOCAs), and contributes substantially to heart failure with preserved ejection fraction (HFpEF). Moving beyond conventional risk-factor stratification, this review dissects the mechanistic pathways through which individual comorbidities compromise coronary microcirculatory integrity. In hypertension, increased mechanical wall stress activates proinflammatory Nuclear factor κB (NF-κB)-mitogen-activated protein kinases (MAPK) signaling cascades. In contrast, in diabetes, chronic hyperglycemia drives microvascular injury through the reactive oxygen species (ROS)-advanced glycation end-products (AGEs) axis and Protein Kinase C (PKC)-dependent pathways. In obesity, adipokine dysregulation and gut-derived metabolites, notably trimethylamine N-oxide (TMAO), promote NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, a central mechanism in obesity-related CMD. In the setting of heart failure (HF) and cardiomyopathies, damage-associated molecular pattern (DAMP)-Toll-like receptor (TLR) interactions and TGF-β/Smad signaling promote capillary rarefaction and interstitial fibrosis, thereby linking systemic inflammation to structural microvascular remodeling. Furthermore, both autoimmune-mediated endotheliitis and virus-induced cytokine surges reduce nitric oxide (NO) bioavailability and impair coronary flow reserve (CFR). Thus, by integrating emerging therapeutic strategies, including interleukin-1β (IL-1β) antagonists, SGLT2 inhibitors, and selected traditional medicines, we highlight approaches aimed at restoring microvascular homeostasis. Finally, we propose a personalized framework that leverages multi-omics profiling and artificial intelligence (AI) to modulate the inflammatory milieu, positioning inflammation-targeted interventions as a fundamental strategy for CMD prevention and management.
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