Key result
Targeting MAVS attenuates inflammation and cardiac remodelling by linking mitochondrial stress to innate immunity.
Why the study?
Mitochondrial antiviral signalling protein (MAVS) has emerged as a regulatory node linking mitochondrial stress, innate immune signalling, and cardiovascular disease pathogenesis, positioning it as a potential therapeutic target.
Answers are grounded in this paper and cite their sources.
This narrative review highlights mitochondrial antiviral signalling protein (MAVS) as a central regulatory node linking mitochondrial stress to innate immune activation and cell death in cardiovascular diseases, positioning it as a promising target for selective pharmacological modulation.
Mitochondrial antiviral signalling protein (MAVS), also known as interferon-β (IFN-β) promoter stimulator 1 (IPS-1), virus-induced signalling adaptor (VISA), and CARD adaptor inducing IFN-β (CARDIF), has emerged as a regulatory node linking mitochondrial stress, innate immune signalling, and cardiovascular disease (CVD) pathogenesis. In the cardiovascular system, MAVS is activated not only by viral RNA sensors such as retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5), but also by endogenous danger signals. This activation promotes transcription of NLR family pyrin domain-containing 3 (NLRP3) and pro-inflammatory cytokines, and facilitates NLRP3 inflammasome assembly and cytokine maturation, processes implicated in myocardial inflammation, remodelling, and dysfunction in conditions such as myocardial hypertrophy, atherosclerosis, and cardiomyopathy. Beyond inflammasome activation, MAVS intersects with multiple cell death and homeostatic pathways relevant to CVD, including apoptosis, autophagy, and, potentially, ferroptosis. Preclinical studies show that genetic ablation of MAVS, or pharmacological interventions that limit mitochondrial reactive oxygen species (mtROS), mitochondrial double-stranded RNA (mtdsRNA) release, or downstream innate immune signalling, can attenuate MAVS-associated inflammation, oxidative stress, and metabolic remodelling, thereby slowing disease progression in experimental cardiovascular models. MAVS, however, also performs essential protective functions, particularly in antiviral defence and maintenance of cardiac homeostasis, underscoring the need for context-specific, cell-type-restricted, or pathway-selective modulation rather than indiscriminate inhibition. Collectively, these findings position MAVS as a promising therapeutic target in CVD, warranting further investigation into MAVS-associated signalling pathways and their modulation in cardiovascular contexts.
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Mayamba et al. (2026) conducted a review in Cardiovascular diseases (CVD). Mitochondrial antiviral signalling protein (MAVS) modulation was evaluated. Mitochondrial antiviral signalling protein (MAVS) links mitochondrial stress and innate immune pathways, serving as a promising pharmacological target to attenuate inflammation and remodelling in CVD.
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