Sex Differences in Atrial Fibrillation

Tamirisa, Kamala P.; Calvert, Peter; Dye, Cicely; Mares, Adriana; Gupta, Dhiraj; Al‐Ahmad, Amin; Russo, Andrea M.

doi:10.1007/s11886-023-01927-1

Cited by 5 publications

(2 citation statements)

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“…5 Its incidence is higher in men than in women. 6,7 Hypertension, another important public health problem, affects approximately 20-50% of the adult population worldwide, and its prevalence is increasing. 8 AF is associated with hypertension, and patients with hypertension have a 1.7-fold higher risk of developing AF than normotensive patients.…”

Section: Introductionmentioning

confidence: 99%

“…In the Chinese adult population, the prevalence of AF has increased from 0.40% to 0.45% between 2012 and 2017 to approximately 1.6% from 2020 to 2021, 3,4 leading to a significant economic burden 5 . Its incidence is higher in men than in women 6,7 . Hypertension, another important public health problem, affects approximately 20–50% of the adult population worldwide, and its prevalence is increasing 8 .…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of fibromodulin attenuates inflammatory signaling and atrial fibrosis in spontaneously hypertensive rats with atrial fibrillation via inhibiting TLR4/NLRP3 signaling pathway

Liang,

Zhou,

Wang

et al. 2023

Immunity Inflam & Disease

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BackgroundMyocardial fibrosis is an important factor in the induction and maintenance of atrial fibrillation (AF). Fibromodulin (FMOD) promotes fibrotic gene expression. However, its specific role in spontaneously hypertensive rats (SHR)‐AF remains unclear.MethodsWe analyzed FMOD mRNA and protein expression in rat atrial tissues using RT‐qPCR, Western blot analysis, and immunohistochemistry. Histopathological examination of atrial tissues was performed using hematoxylin and eosin (H&E), Masson's trichrome, and Picrosirius red staining. The levels of inflammatory and fibrosis‐related proteins were measured using Western blot analysis.ResultsFMOD relative mRNA and protein expression levels were notably upregulated in atrial tissues of both AF groups (normal‐AF and SHR‐AF groups) than that in atrial tissues of the no‐AF group (normal and SHR group). This effect was particularly pronounced in the SHR‐AF group. Pathological changes revealed that the extracellular matrix, collagen, collagen fibers, and left atrial diameter were notably increased in the atrial tissues from the SHR‐AF group compared to those in the atrial tissues from the SHR group, whereas the left ventricular fractional shortening and left ventricular ejection fraction were notably lower. Expression of TLR4, MyD88, NLRP3, TGF‐β1, collagen I, and collagen II mRNA were clearly higher in atrial tissues from the SHR‐AF group than in those from the SHR group. Protein levels of TLR4, MyD88, NLRP3, Cleavage‐Caspase‐1, Cleavage‐IL‐1β, TGF‐β1, p‐Smad2, collagen I, and collagen II were clearly higher in atrial tissues from the SHR‐AF group than in those from the SHR group. FMOD knockdown inhibited atrial fibrosis, collagen accumulation, and the TLR4/MyD88/NLRP3 signaling pathway.ConclusionDownregulation of FMOD attenuated inflammatory signaling and atrial fibrosis in SHR‐AF by inhibiting the TLR4/NLRP3 signaling pathway. Therefore, FMOD may be a promising therapeutic target in AF.

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