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 investigate the impact of interleukin-17(IL-17D)knockout on lipid phagocytosis in ath-erosclerosis(AS)and bone marrow-derived macrophages.METHODS:Twenty 8-week-old ApoE-/-C57BL/6J mice were randomly assigned to experimental and control groups(10 mice per group).The experimental group was subjected to a high-fat diet for 8 weeks to induce AS,while the control group received a normal diet.Additionally,fifteen 8-week-old ApoE-/-IL-17D-/-and ApoE-/-mice were also fed a high-fat diet for the same duration.Body weight and blood lipid levels were measured.Aortas were harvested,and IL-17D expression was assessed using RT-qPCR.Bone marrow cells were iso-lated and differentiated into macrophages with colony-stimulating factors.Oil red O staining was employed to visualize lip-id deposition in aortic plaques and macrophages.To stimulate macrophages,oxidized low-density lipoprotein(oxLDL)was used,and RT-qPCR along with Western blot analyses were conducted to evaluate the expression of lipid phagocytosis-related genes and the p38 MAPK signaling pathway.Dehydrocorydaline(DHC),a p38 MAPK activator,was adminis-tered to IL-17D-/-macrophages,and the expression of CD36 and lipid phagocytosis were assessed.RESULTS:IL-17D ex-pression was significantly elevated in the aortas of AS mice and in oxLDL-treated macrophages(P<0.01).IL-17D-/-mice exhibited notably lower serum total cholesterol and low-density lipoprotein cholesterol levels(P<0.01),along with a sig-nificant reduction in plaque area in the aortas and aortic roots(P<0.01).Macrophages lacking IL-17D demonstrated de-creased expression of CD36,LOX-1,IL-1β,and IL-6(P<0.01)and showed diminished lipid phagocytosis.These mac-rophages also exhibited reduced phosphorylation of p38(P<0.01)compared to wild-type macrophages.Activation of p38 MAPK by DHC significantly countered the inhibitory effects of IL-17D knockout on CD36 expression(P<0.01)and en-hanced lipid phagocytosis in macrophages.CONCLUSION:Knockout of IL-17D may modulate lipid phagocytosis in macro-phages via the p38/CD36 signaling pathway,potentially inhibiting the formation and progression of aortic plaques in mice.

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 investigate the impact of interleukin-17(IL-17D)knockout on lipid phagocytosis in ath-erosclerosis(AS)and bone marrow-derived macrophages.METHODS:Twenty 8-week-old ApoE-/-C57BL/6J mice were randomly assigned to experimental and control groups(10 mice per group).The experimental group was subjected to a high-fat diet for 8 weeks to induce AS,while the control group received a normal diet.Additionally,fifteen 8-week-old ApoE-/-IL-17D-/-and ApoE-/-mice were also fed a high-fat diet for the same duration.Body weight and blood lipid levels were measured.Aortas were harvested,and IL-17D expression was assessed using RT-qPCR.Bone marrow cells were iso-lated and differentiated into macrophages with colony-stimulating factors.Oil red O staining was employed to visualize lip-id deposition in aortic plaques and macrophages.To stimulate macrophages,oxidized low-density lipoprotein(oxLDL)was used,and RT-qPCR along with Western blot analyses were conducted to evaluate the expression of lipid phagocytosis-related genes and the p38 MAPK signaling pathway.Dehydrocorydaline(DHC),a p38 MAPK activator,was adminis-tered to IL-17D-/-macrophages,and the expression of CD36 and lipid phagocytosis were assessed.RESULTS:IL-17D ex-pression was significantly elevated in the aortas of AS mice and in oxLDL-treated macrophages(P<0.01).IL-17D-/-mice exhibited notably lower serum total cholesterol and low-density lipoprotein cholesterol levels(P<0.01),along with a sig-nificant reduction in plaque area in the aortas and aortic roots(P<0.01).Macrophages lacking IL-17D demonstrated de-creased expression of CD36,LOX-1,IL-1β,and IL-6(P<0.01)and showed diminished lipid phagocytosis.These mac-rophages also exhibited reduced phosphorylation of p38(P<0.01)compared to wild-type macrophages.Activation of p38 MAPK by DHC significantly countered the inhibitory effects of IL-17D knockout on CD36 expression(P<0.01)and en-hanced lipid phagocytosis in macrophages.CONCLUSION:Knockout of IL-17D may modulate lipid phagocytosis in macro-phages via the p38/CD36 signaling pathway,potentially inhibiting the formation and progression of aortic plaques in mice.

Objective To explore the clinical efficacy and nursing experience of the mild moxibustion combined with acupoint massage therapy on the urinary retention patients after orthopedic surgery . Methods Sixty-eight urinary retention patients after orthopedic surgery from January 2012 to April 2013 were chosen and divided into the control group and the observation group according to the random number table , each with 34 cases.The control group received the routine induced urination , and the observation group received the mild moxibustion combined with acupoint massage .The clinical efficacy , the significantly effective and effective times of micturition were observed and compared in two groups .Results The total effective rate , the significantly effective and effective times of micturition were respectively 85.3%, (21.0 ±5.0) min, (34.0 ±6.0) min in the observation group, and were 55.9%, (29.0 ±6.0) min, (39.0 ±7.0) min in the observation group, and the differences were statistically significant (χ2 =7.08,t=2.81,2.64, respectively;P<0.05).Conclusions The mild moxibustion combined with acupoint massage therapy on the urinary retention patients after orthopedic surgery can significantly increase the clinical efficacy , and improve the prognosis of patients , and is worthy of clinical promotion .