Key result
Toll-like receptors mediate inflammatory responses that contribute to pathological cardiac hypertrophy, making TLR signaling pathways potential therapeutic targets.
Why the study?
Targeting TLR signaling might be an effective strategy against pathological cardiac hypertrophy, making it necessary to study the mechanisms underlying TLR functions in hypertrophic remodeling.
This review summarizes the mechanisms underlying Toll-like receptor (TLR) signaling in the development of pathological cardiac hypertrophy.
TLR signaling may link inflammation to hypertrophy and HF progression; extends mechanistic data but leaves open clinical translation.
Toll-like receptors (TLRs) are a family of pattern recognition receptors (PRRs) that can identify pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). TLRs play an important role in the innate immune response, leading to acute and chronic inflammation. Cardiac hypertrophy, an important cardiac remodeling phenotype during cardiovascular disease, contributes to the development of heart failure. In previous decades, many studies have reported that TLR-mediated inflammation was involved in the induction of myocardium hypertrophic remodeling, suggesting that targeting TLR signaling might be an effective strategy against pathological cardiac hypertrophy. Thus, it is necessary to study the mechanisms underlying TLR functions in cardiac hypertrophy. In this review, we summarized key findings of TLR signaling in cardiac hypertrophy.
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Zhang et al. (2023) conducted a review in Cardiac hypertrophy. Toll-like receptor (TLR) signaling modulators was evaluated. Toll-like receptors mediate inflammatory responses that contribute to pathological cardiac hypertrophy, making TLR signaling pathways potential therapeutic targets.
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