Cardiovascular disease(CVD)is a leading cause of death worldwide,posing a substantial burden on so-ciety.Transfer RNA-derived fragment(tRF)is a novel class of non-coding small RNA produced primarily through the specific cleavage of precursor or mature transfer RNA(tRNA).Unlike the canonical role of tRNA in amino acid trans-port,tRF plays important roles in regulating gene transcription,translation,and epigenetic modifications,thereby influen-cing pathophysiological processes such as cell proliferation,differentiation,and apoptosis.In recent years,with the wide-spread application of small RNA sequencing technologies,a growing number of studies have demonstrated close associations between tRF and the development and progression of various CVDs,making them a research hotspot in the field.This re-view systematically summarizes the origin,classification,functional mechanisms,and recent advances in tRF research re-lated to CVD,aiming to provide new directions for understanding the pathogenesis of CVD and identifying potential thera-peutic targets.

Cardiovascular disease(CVD)is a leading cause of death worldwide,posing a substantial burden on so-ciety.Transfer RNA-derived fragment(tRF)is a novel class of non-coding small RNA produced primarily through the specific cleavage of precursor or mature transfer RNA(tRNA).Unlike the canonical role of tRNA in amino acid trans-port,tRF plays important roles in regulating gene transcription,translation,and epigenetic modifications,thereby influen-cing pathophysiological processes such as cell proliferation,differentiation,and apoptosis.In recent years,with the wide-spread application of small RNA sequencing technologies,a growing number of studies have demonstrated close associations between tRF and the development and progression of various CVDs,making them a research hotspot in the field.This re-view systematically summarizes the origin,classification,functional mechanisms,and recent advances in tRF research re-lated to CVD,aiming to provide new directions for understanding the pathogenesis of CVD and identifying potential thera-peutic targets.

AIM: To clarify the role of nitric oxide (NO) system in development of chronic hypoxic hypercapnic pulmonary hepertension. METHODS: Male Sprague-Dawley rats were randomly divided into control group and hypoxic hypercapnic group. NO content of plasma was determined, constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) were examined using the technique of immunohistochemistry, expression of cNOS mRNA and iNOS mRNA of arteriole were detected by in situ hybridization. RESULTS: Plasma NO concentration, cNOS activity and cNOS mRNA expression in arteriole of chronic hypoxic hypecapnic group were significantly lower than that of control group ( P

AIM: To investigate the effect of diltiazem on mean pulmonary arterial pressure(mPAP) and nitric oxide synthase(NOS) in arterioles in chronic hypoxic hypercapnic rats. METHODS: Twenty-four rats were randomly divided into three groups: control group(A),hypoxic hypercapnic group(B), hypoxic hypercapnia+ diltiazem group (C), constitutive endothelial NOS(ceNOS) were observed in arterioles of rats using the technique of immunohistochemistry,ceNOS mRNA were observed by the technique of in situ hybridization . RESULTS: (1)mPAP was significantly higher in rats of B group than that of A and C group( P 0 05),but mCAP was lower in rats of C group than that in B group.(2)Light microscopy showed WA/TA (vessel wall area/total area) was significantly lower in rats of C group than that of B group ( P

AIM: To investigate the expression of soluble guanylate cyclase protein and its mRNA in rat pulmonary artery after exposure to hypoxia and hypercapnia. METHODS: Male Sprague-Dawley rats were randomly split into 4 group, which were hypoxic hypercapnic (HH 1 week, HH 2 weeks, HH 4 weeks) group and control group, to copy pulmonary hypertensive animal model. The expression of sGC? 1 and ? 1 subunits protein of medial and small pulmonary artery was performed by immunohistochemistry with a polycolonal antibody. In situ hybridization was performed on the rat lung tissue using sGC oligonuclear probe to assay the expression of sGC? 1 subunit mRNA. RESULTS: The sGC? 1 and ? 1 subunits protein and sGC? 1 subunit mRNA were faint staining in the pulmonary small and medium artery in HH1 week, HH 2 weeks and HH 4 weeks groups compared with control group (all P