Reduce Tissue Damage Research Articles

Understanding the Role of Purinergic P2X7 Receptors in the Gastrointestinal System: A Systematic Review.

Background: The role of purinergic P2X7 receptor (P2X7R) is of interest due to its involvement in inflammation and mediating immune cell responses. P2X7R is particularly implicated in the development of inflammatory bowel disease (IBD). However, the extent of the actions of P2X7R in the gastrointestinal (GI) system under physiological and pathophysiological conditions remains to be elucidated. This systematic review aimed to identify, summarize and evaluate the evidence for a critical role of P2X7R in the GI system. Methods: We searched PubMed, Embase and Scopus with search terms pertained to P2X7R in the GI system in disease or physiological state, including “P2X7 or P2X7 receptor or purinergic signaling” in combination with any of the terms “intestine or colon or gut or gastrointestinal,” “pathology or inflammation or disease or disorder,” and “physiology or expression.” Titles and abstracts were screened for potentially eligible full texts, and animal and human studies published in English were included in this study. Data were extracted from papers meeting inclusion criteria. Meta-analysis was not feasible given the study diversity. Results: There were 48 papers included in this review. We identified 14 experimental colitis models, three sepsis models and one ischemia-reperfusion injury model. Among them, 11 studies examined P2X7R in GI infections, six studies on immune cell regulation, four studies on GI inflammation, two studies on GI malignancies, three studies involving intestinal injury due to various causes, two studies on ATP-activated P2X7R in the GI system and two studies on metabolic regulation. Conclusion: Evidence supports P2X7R mediating inflammation and immune cell responses in GI inflammation, infections and injury due to IBD and other challenges to the intestinal wall. P2X7R inhibition by gene knockout or by application of P2X7R antagonists can reduce tissue damage by suppressing inflammation. P2X7R is also implicated in GI malignancies and glucose and lipid homeostasis. P2X7R blockade, however, did not always lead to beneficial outcomes in the various pathological models of study.

Long-term adaptation following influenza A virus host shifts results in increased within-host viral fitness due to higher replication rates, broader dissemination within the respiratory epithelium and reduced tissue damage

The mechanisms and consequences of genome evolution on viral fitness following host shifts are poorly understood. In addition, viral fitness -the ability of an organism to reproduce and survive- is multifactorial and thus difficult to quantify. Influenza A viruses (IAVs) circulate broadly among wild birds and have jumped into and become endemic in multiple mammalian hosts, including humans, pigs, dogs, seals, and horses. H3N8 equine influenza virus (EIV) is an endemic virus of horses that originated in birds and has been circulating uninterruptedly in equine populations since the early 1960s. Here, we used EIV to quantify changes in infection phenotype associated to viral fitness due to genome-wide changes acquired during long-term adaptation. We performed experimental infections of two mammalian cell lines and equine tracheal explants using the earliest H3N8 EIV isolated (A/equine/Uruguay/63 [EIV/63]), and A/equine/Ohio/2003 (EIV/2003), a monophyletic descendant of EIV/63 isolated 40 years after the emergence of H3N8 EIV. We show that EIV/2003 exhibits increased resistance to interferon, enhanced viral replication, and a more efficient cell-to-cell spread in cells and tissues. Transcriptomics analyses revealed virus-specific responses to each virus, mainly affecting host immunity and inflammation. Image analyses of infected equine respiratory explants showed that despite replicating at higher levels and spreading over larger areas of the respiratory epithelium, EIV/2003 induced milder lesions compared to EIV/63, suggesting that adaptation led to reduced tissue pathogenicity. Our results reveal previously unknown links between virus genotype and the host response to infection, providing new insights on the relationship between virus evolution and fitness.

Attenuating ischemia-reperfusion injury with polymerized albumin.

Ischemia-reperfusion injury increased vascular permeability, resulting in fluid extravasation from the intravascular compartment into the tissue space. Fluid and small protein extravasation lead to increased interstitial fluid pressure and capillary collapse, impairing capillary exchange. Polymerized human serum albumin (PolyHSA) has an increased molecular weight (MW) compared with unpolymerized human serum albumin (HSA) and can improve intravascular fluid retention and recovery from ischemia-reperfusion injury. To test the hypothesis that polymerization of HSA can improve recovery from ischemia-reperfusion injury, we studied how exchange transfusion of 20% of the blood volume with HSA or PolyHSA immediately before reperfusion can affect local ischemic tissue microhemodynamics, vascular integrity, and tissue viability in a hamster dorsal window chamber model. Microvascular flow and functional capillary density were maintained in animals exchanged with PolyHSA compared with HSA. Likewise, exchange transfusion with PolyHSA preserved vascular permeability measured with extravasation of fluorescently labeled dextran. The intravascular retention time of the exchanged PolyHSA was significantly longer compared with the intravascular retention time of HSA. Lastly, the viability of tissue subjected to ischemia-reperfusion injury increased in animals exchanged with PolyHSA compared with HSA. Therefore maintenance of microvascular perfusion, improvement in vascular integrity, and reduction in tissue damage resulting from reperfusion with PolyHSA suggest that PolyHSA is a promising fluid therapy to improve outcomes of ischemia-reperfusion injury.NEW & NOTEWORTHY Polymerized human serum albumin reduced reperfusion injury and preservers microvascular hemodynamics. Polymerized human serum albumin reduces fluid extravasation and prevents fluid extravasation. Consequently, the tissue viability of ischemic tissue is preserved by polymerized human serum.

Highlights from Recent Cancer Literature

Highlights from Recent Cancer Literature

Muscle Derived Mesenchymal Stem Cells Inhibit the Activity of the Free and the Neutrophil Extracellular Trap (NET)-Bond Myeloperoxidase.

Mesenchymal stem cells (MSCs) are known to migrate to tissue injury sites to participate in immune modulation, tissue remodelling and wound healing, reducing tissue damage. Upon neutrophil activation, there is a release of myeloperoxidase (MPO), an oxidant enzyme. But little is known about the direct role of MSCs on MPO activity. The aim of this study was to investigate the effect of equine mesenchymal stem cells derived from muscle microinvasive biopsy (mdMSC) on the oxidant response of neutrophils and particularly on the activity of the myeloperoxidase released by stimulated equine neutrophils. After specific treatment (trypsin and washings in phosphate buffer saline), the mdMSCs were exposed to isolated neutrophils. The effect of the suspended mdMSCs was studied on the ROS production and the release of total and active MPO by stimulated neutrophils and specifically on the activity of MPO in a neutrophil-free model. Additionally, we developed a model combining adherent mdMSCs with neutrophils to study total and active MPO from the neutrophil extracellular trap (NET). Our results show that mdMSCs inhibited the ROS production, the activity of MPO released by stimulated neutrophils and the activity of MPO bound to the NET. Moreover, the co-incubation of mdMSCs directly with MPO results in a strong inhibition of the peroxidase activity of MPO, probably by affecting the active site of the enzyme. We confirm the strong potential of mdMSCs to lower the oxidant response of neutrophils. The novelty of our study is an evident inhibition of the activity of MPO by MSCs. The results indicated a new potential therapeutic approach of mdMSCs in the inhibition of MPO, which is considered as a pro-oxidant actor in numerous chronic and acute inflammatory pathologies.

Finafloxacin, a Novel Fluoroquinolone, Reduces the Clinical Signs of Infection and Pathology in a Mouse Model of Q Fever.

Finafloxacin is a novel fluoroquinolone with optimal antibacterial activity in low pH environments, therefore offering a therapeutic advantage over some traditional antibiotics, in treating bacterial infections associated with acidic foci. Coxiella burnetii, the causative agent of Q fever, is a bacterium which resides and replicates in acidic intracellular parasitic vacuoles. The efficacy of finafloxacin was evaluated in vivo using the A/J mouse model of inhalational Q fever and was compared to doxycycline, the standard treatment for this infection and ciprofloxacin, a comparator fluoroquinolone. Finafloxacin reduced the severity of the clinical signs of infection and weight loss associated with Q fever, but did not reduce the level of bacterial colonization in tissues compared to doxycycline or ciprofloxacin. However, histopathological analysis suggested that treatment with finafloxacin reduced tissue damage associated with C. burnetii infection. In addition, we report for the first time, the use of viable counts on axenic media to evaluate antibiotic efficacy in vivo.

Abstract 11322: Role of Centhaquine (lyfaquin ® ) in the Protection of Renal Tissues After Acute Kidney Injury

Background: Acute Kidney Injury (AKI) is frequently associated with an in-hospital complication of sepsis, heart conditions, hemorrhagic shock, and surgery. However, at present, no specific drug to treat AKI is available. Centhaquine (Lyfaquin ® ) is a safe and effective first-in-class resuscitative agent for hypovolemic shock. We are investigating whether centhaquine could protect kidneys from acute injury during hypovolemic shock. Hypothesis: AKI is known to be associated with shock-related morbidity and mortality. We hypothesize that centhaquine would have a direct effect on alleviating the AKI and reducing shock-related mortality. Methods: Renal arteries of rats were clamped and de-clamped to induce AKI like ischemia/reperfusion model, and hemorrhage was carried out by withdrawing blood for 30 min from the femoral artery. Rats were resuscitated with centhaquine (0.02 mg/kg) for 10 min. Mean Arterial Pressure (MAP), heart rate (HR), and renal blood flow (RBF) were monitored for 120 min. Results: An improved RBF (p<0.003) in centhaquine compared to vehicle rats was observed after resuscitation. While MAP and HR were similar in centhaquine and vehicle groups. At 120 min post-resuscitation, significantly reduced blood lactate level (p=0.0064) in centhaquine than the vehicle was seen. Higher damage in renal tissues in the vehicle than centhaquine was observed by histopathological analysis. Western blots showed higher HIF-1α (p=0.0152) and lower NGAL (p=0.01626) levels in centhaquine vs. vehicle. While significantly higher (p<0.045) expression of HIF-1α and lower expression of Bax (p<0.044) in kidney cortex and medulla of centhaquine rats were observed after immunofluorescence analysis. On the other hand, expression of PHD 3 (p<0.0001) was higher, while the expression of Cytochrome C (p=0.01429) was lower in the cortex of centhaquine than the vehicle. Also, the in situ PCR data showed higher mitochondrial biogenesis in centhaquine than in the vehicle. Conclusions: Centhaquine (Lyfaquin ® ) increases renal blood flow and augments hypoxia response, which probably helps reduce tissue damage and apoptosis following hemorrhagic shock induced AKI, and hence the potential of centhaquine could be explored further to prevent/treat AKI.

Mast cell activation disease and immunoglobulin deficiency in patients with hypermobile Ehlers-Danlos syndrome/hypermobility spectrum disorder.

Mast cell activation disease (MCAD) includes single organ disease such as asthma, urticaria, and gastroenteritis, as well as multiorgan system involvement such as mast cell activation syndrome and anaphylaxis. Reports link MCAD with hypermobile Ehlers-Danlos syndrome (hEDS), hypermobility spectrum disorder (HSD), and with primary immune deficiencies such as complement and immunoglobulin deficiencies (Ig Def). This study assesses the concurrence of these syndromes. We undertook a cohort analysis of patients seen in a community-based Allergy/Immunology clinic from 2015 to 2019. We searched for diagnostic codes for Ig Def disorders, hypermobility syndrome, hypermobile/Ehlers-Danlos syndrome, and MCADs. Of 974 patients with suspected MCAD, 449 (46%) had a diagnosis of MCAD; 496 (51%) of cases had a combination of at least two of hEDS/HSD, MCAD, and Ig Def. Ig Def was present in 417 (43%) of patients; 188 (19.3%) had hEDS/HSD with an Ig Def with or without MCAD and accounted for 45% of all the cases with Ig Def. Of 974 cases, 101 (10%) had hEDS/HSD and MCAD; 207 (21%) had Ig Def and MCAD; 7 (0.7%) had Ig Def and hEDS/HSD; and 181 (19%) had a combination of all three syndromes. Most patients (74%) with these comorbidities were female. The presence of MCAD and Ig Def should be explored in patients with hEDS/HSD. Identifying underlying contributors to recurrent/chronic inflammation and tissue injury is needed to tailor and personalize therapies. This, in turn, can reduce tissue damage, iatrogenic intervention, and optimize health outcomes.

Evaluation of probiotic bacteria Leucosnostoc mensenteroides against White Gut Disease in shrimp aquaculture

With increasing demand for environment friendly aquaculture, use of beneficial bacteria to displace pathogens by competitive processes is being used in the animal industry as a better remedy and is now gaining acceptance for pathogen control in aquaculture. With this concern, the present study was designed for isolation of suitable probiotic bacteria from natural sources, application in an effective dose in the rearing environment is expected to control the blowout of White Gut Disease in aquaculture systems. The interaction of pathogenic Vibrio anguillarum and the inner surface of the digestive tract of P. monodon, with a specific focus on their in-situ morphology, aggregation and attachment characteristics presented with pathogenic bacterial species and under the control of probiotic bacteria were analyzed through. The percentage of granular cells of treated group was higher than the control. Histological studies revealed that the treated group has optimistic effect which helps in the reduction of tissue damage and decrease the mortality rate than the infected shrimps. Leuconostoc sp., can survive in the saline condition rather than other Lactobacillus sp., and its tolerance of acidic environment of the shrimp intestine and their adherence level at the intestine will progressively replace the V. anguillarum from the infected shrimps and commendably control the White Gut Disease.

L-theanine relieves acute alcoholic liver injury by regulating the TNF-α/NF-κB signaling pathway in C57BL/6J mice

Acute alcoholic liver injury (AALI) refers to the inflammatory hepatic damage caused by alcohol. In severe cases, it can lead to steatohepatitis, alcoholic fibrosis and even cirrhosis. In this study, we analyzed the hepatoprotective activity of L-theanine on mice fed with a large amount of ethanol at one time, and the underlying molecular mechanism. The extensive liver injury caused by alcohol feeding was alleviated by L-theanine, which reduced tissue damage, decreased transaminase levels, and increased antioxidant activity. Mechanistically, L-theanine downregulated phosphorylated NF-κB, TNF-α and IKKα in the liver tissues and the LO2 normal hepatocyte cell line, which in turn lowered secretion of iNOS, IL-1β and IL-6. Taken together, L-theanine prevents alcohol-induced liver inflammation by blocking the intrahepatic TNF-α/NF-κB pathway, and is a promising treatment strategy against AALI.

Impact of C57BL/6J and SV-129 Mouse Strain Differences on Ischemia-Induced Postnatal Angiogenesis and the Associated Leukocyte Infiltration in a Murine Hindlimb Model of Ischemia.

Strain-related differences in arteriogenesis in inbred mouse strains have already been studied excessively. However, these analyses missed evaluating the mouse strain-related differences in ischemia-induced angiogenic capacities. With the present study, we wanted to shed light on the different angiogenic potentials and the associated leukocyte infiltration of C57BL/6J and SV-129 mice to facilitate the comparison of angiogenesis-related analyses between these strains. For the induction of angiogenesis, we ligated the femoral artery in 8–12-week-old male C57BL/6J and SV-129 mice and performed (immuno-) histological analyses on the ischemic gastrocnemius muscles collected 24 h or 7 days after ligation. As evidenced by hematoxylin and eosin staining, C57BL/6J mice showed reduced tissue damage but displayed an increased capillary-to-muscle fiber ratio and an elevated number of proliferating capillaries (CD31+/BrdU+ cells) compared to SV-129 mice, thus showing improved angiogenesis. Regarding the associated leukocyte infiltration, we found increased numbers of neutrophils (MPO+ cells), NETs (MPO+/CitH3+/DAPI+), and macrophages (CD68+ cells) in SV-129 mice, whereas macrophage polarization (MRC1- vs. MRC1+) and total leukocyte infiltration (CD45+ cells) did not differ between the mouse strains. In summary, we show increased ischemia-induced angiogenic capacities in C57BL/6J mice compared to SV-129 mice, with the latter showing aggravated tissue damage, inflammation, and impaired angiogenesis.

Azithromycin reduces inflammation-amplified hypoxic-ischemic brain injury in neonatal rats.

Background:Systemic inflammation amplifies neonatal hypoxic-ischemic (HI) brain injury. Azithromycin (AZ), an antibiotic with anti-inflammatory properties, improves sensorimotor function and reduces tissue damage after neonatal rat HI brain injury.Objective:To determine if AZ is neuroprotective in two neonatal rat models of inflammation-amplified HI brain injury.Design/Methods:Seven-day-old (P7) rats received injections of toll-like receptor agonists lipopolysaccharide (LPS) or Pam3Cys-Ser-(Lys)4 (PAM) prior to right carotid ligation followed by 50 min (LPS+HI) or 60 min (PAM+HI) in 8% oxygen. Outcomes included contralateral forelimb function (forepaw placing; grip strength), survival, %intact right hemisphere (brain damage), and a Composite Score incorporating these measures. We compared P35 outcomes in controls and groups treated with 3 or 5 AZ doses. Then, we compared P21 outcomes when the first (of 5) AZ doses was administered 1, 2, or 4 hours after HI.Results:In both LPS+HI and PAM+HI models, AZ improved sensorimotor function, survival, brain tissue preservation, and Composite Scores. Benefits increased with 5 vs. 3-dose AZ and declined with longer initiation delay.Conclusion:Perinatal systemic infection is a common comorbidity of neonatal asphyxia brain injury and contributes to adverse outcomes. These data support further evaluation of AZ as a candidate treatment for neonatal neuroprotection.

Artesunate strongly modulates myeloid and regulatory T cells to prevent LPS-induced systemic inflammation

Lipopolysaccharide (LPS) is the major component of the outer membrane of Gram-negative bacteria and is usually administrated to establish models of inflammation. Artesunate (ART), a water-soluble artemisinin derivative, displays multiple pharmacological actions against tumors, viral infections, and inflammation, and has been used as a therapeutic weapon against malaria. In this study, our aim was to evaluate whether ART pretreatment is capable of preventing inflammation induced by LPS. BALB/c mice were treated with 100 mg/kg of ART i.p. for 7 days followed by a single dose of LPS. ART pretreatment led to an improvement in clinical score, prevented alterations in biochemical markers, and reestablished the platelet counts. Flow cytometry analysis showed that ART protected the inflammation mainly by reducing the percentage of M1 macrophages while increasing M2 macrophages and a reestablishment of classical monocytes in the BM. In the spleen, ART pretreatment increased N2 neutrophils, myeloid-derived suppressor cells (MDSC), and regulatory T cells, the latter was also increased in peripheral blood. In addition, a marked decrease in inflammatory cytokines and chemokines was observed in the ART treated group. Our data suggest that ART prevents inflammation, reducing tissue damage and restoring homeostasis.

Histopatology of Cyprinus carpio tissue infected by Aeromonas hydrophila in profilactical therapy Pothos tener Wall

Photos tener Wall is a semi-aquatic plant that lives in the Bantimurung waterfall, South Sulawesi. The aims of study to determine the effectiveness of P. tener Wall in prophylactic therapy against Aeromonas hydrophila infection in Cyprinus carpio. The treatment procedures were: a) Soaking the live P. tener Wall in aquarium at a dose of 15 gr, 30 gr, 60 gr wet weight, b) Provision of P. tener Wall through feed at a dose of 1%, 2% and 4%, c) mixed treatment of 30 gr P. tener Wall live and 4% P. tener Wall in feed. Positive control (d) C. carpio given oxytetracyline antibiotics and negative control (e) C. carpio without P. tener Wall treatment and without antibiotics. Histological observations of liver, kidney and lymph were carried out: a) Before prophylactic therapy (as a normal condition), b) 30th day of prophylactic therapy c) 7th day after A. hydrophila infection. The results of histological observations showed that C, carpio in normal condition. Treatment with oxytetracyline antibiotics showed a lot of tissue damage, fatty degeneration, haemorrhage, and no necrosis. Negative controls included more necrosis, fatty degeneration, tissue damage, haemorrhage, hyperplasia. The P. tener wall treatment had little of tissue damage compared to positive and negative controls. Conclusion Prophylactic therapy with P. tener Wall can emphasize and reduce tissue damage caused by A. hydrophila attack rather than antibiotic treatment.

Force from Shape—Estimating the Location and Magnitude of the External Force on Flexible Instruments

Force sensing is highly desirable in minimally invasive medical applications, since this feature shows great potential for reducing tissue damage and enhancing manipulation safety. However, embedding force sensors in medical devices is challenging and costly. This article explores the possibility to use shape sensing as a measure to extract force information. In this work, a model-based approach that allows simultaneous shape and force sensing is proposed. Shape information is reconstructed employing a multicore fiber with fiber Bragg grating sensors spaced over the fiber length. This fiber is capable of distributed 3D shape sensing. It is shown how by making use of extended Kalman filter and a mechanics model of the flexible instrument, it becomes possible to estimate both the magnitudes and locations of externally applied forces. Experiments were carried out to validate the proposed method for both one and two external forces applied at arbitrary locations in different directions on a flexible instrument. Results show that one-directional force magnitude and location can be estimated with an average error of 23.08 mN (15.39%) and 11.06 mm (6.51%), respectively. For two-directional forces, results of the load near the base show an average error of 52.01 mN (30.59%) for the magnitude and 29.24 mm (17.20%) for the location. For the load applied simultaneously near the tip, the mean magnitude error is 16.79 mN (11.19%) and the average location error is 10.18 mm (5.99%). The force sensing algorithm can run in real time with an approximate frequency of 59 Hz. In these experiments, it can be observed that the force-sensing accuracy, which depends on the sensitivity of the shape of flexible instruments with respect to the external force, can vary drastically in function of the force application point and force direction.

Immunoregulatory Functions of Interferons During Genital HSV-2 Infection.

Herpes simplex virus type 2 (HSV-2) infection is one of the most prevalent sexually transmitted infections that disproportionately impacts women worldwide. Currently, there are no vaccines or curative treatments, resulting in life-long infection. The mucosal environment of the female reproductive tract (FRT) is home to a complex array of local immune defenses that must be carefully coordinated to protect against genital HSV-2 infection, while preventing excessive inflammation to prevent disease symptoms. Crucial to the defense against HSV-2 infection in the FRT are three classes of highly related and integrated cytokines, type I, II, and III interferons (IFN). These three classes of cytokines control HSV-2 infection and reduce tissue damage through a combination of directly inhibiting viral replication, as well as regulating the function of resident immune cells. In this review, we will examine how interferons are induced and their critical role in how they shape the local immune response to HSV-2 infection in the FRT.

Cardioporation enhances myocardial gene expression in rat heart

Damage from myocardial infarction (MI) and subsequent heart failure are serious public health concerns. Current clinical treatments and therapies to treat MI damage largely do not address the regeneration of cardiomyocytes. In a previous study, we established that it is possible to promote regeneration of cardiac muscle with vascular endothelial growth factor B gene delivery directly to the ischemic myocardium. In the current study we aim to optimize cardioporation parameters to increase expression efficiency by varying electrode configuration, applied voltage, pulse length, and plasmid vector size. By using a surface monopolar electrode, optimized pulsing conditions and reducing vector size, we were able to prevent ventricular fibrillation, increase survival, reduce tissue damage, and significantly increase gene expression levels.

Candida albicans Secreted Aspartic Protease 7 is Essential for Damage of Human Oral Epithelial Cells

Aims: Candida albicans is an important human fungal pathogen in clinical settings. It possesses a wide spectrum of virulence traits, including but not limited to the production of Secreted Aspartic Proteases (SAPs), to invade host cells under predisposing conditions. The aims of the present study were to investigate the functional role of C. albicans SAP7 in invasion ability. Methods: The present study was carried out to construct C. albicans sap7Δ/Δ mutant strain using a PCR-based gene disruption method. The behaviors of this SAP7 knockout strain was evaluated and compared with the wild type and SAP7 complemented strains between human oral epithelial cells with respect to endocytosis, invasion, and tissue damage. Results: Compared with the wild type C. albicans strain, a 52% reduction in the endocytosis of the sap7Δ/Δ mutant strain by oral epithelial cells was observed, as well as a 25% attenuation of internalization, and a 27% reduction of tissue damage (P<0.05). Conclusion: Our data clearly demonstrates that C. albicans SAP7 contributes to tissue invasion into human oral epithelial cells which warrant further investigations as potential targets for antifungal interventions.

Research progress of full endoscopic transforaminal lumbar interbody fusion

Full endoscopic transforaminal lumbar interbody fusion has been used widely in the field of minimally invasive spine surgery in recent years. This paper briefly introduces the development history, technical points, indications, curative effects and complications. Authors believe that the full endoscopic transforaminal lumbar interbody fusion has the same clinical effects as traditional surgery, and can effectively reduce tissue damage and intraoperative bleeding, reduce the incidence of postoperative low back pain, shorten the time to get out of bed, and reduce the average hospitalization time. However, it is still necessary to improve the long-term follow up in order to further evaluate the effectiveness and safety of the procedure.

A Systematic Review and Meta-Analysis of the SuperPATH Approach in Hip Arthroplasty.

Objective To compare the clinical and radiographic results of the supercapsular percutaneously assisted total hip (SuperPATH) approach and the conventional approach in hip arthroplasty. Design Based on a prepublished protocol (PROSPERO: CRD42020177717), we searched PubMed, Embase, and Cochrane for relevant literatures up to January 30, 2021. The methodological qualities were assessed using the guidelines provided by the Cochrane Collaboration for Systematic Reviews. Randomized- or fixed-effect models were used to calculate the weighted mean difference (WMD) or odds ratio (OR), respectively, for continuous and dichotomous variables. Results 6 articles were included in the study, and 526 patients were selected, which included 233 cases in the SuperPATH groups and 279 cases in the conventional groups, and 4 cases performed two surgeries in succession. The SuperPATH group demonstrated shorter incision length (WMD = −7.87, 95% CI (−10.05, −5.69), P < 0.00001), decreased blood transfusion rate (OR = 0.48, 95% CI (0.25, 0.89), P = 0.02), decreased visual analogue scale (VAS) (WMD = −0.40, 95% CI (−0.72, −0.08), P = 0.02), and higher Harris hip score (HHS) (WMD = 1.98, 95% CI (0.18, 3.77), P = 0.03) than the conventional group. However, there was no difference in VAS (P = 0.14) and HHS (P = 0.86) between the two groups 3 months later, nor in the acetabular abduction angle (P = 0.32) in either group. Conclusions SuperPATH, as a minimally invasive approach with its reduced tissue damage, quick postoperative recovery, and early rehabilitation, demonstrates the short-term advantages of hip arthroplasty. As the evidences in favor of the SuperPATH technique were limited in a small number of studies and short duration of follow-up, more research is required to further analyze its long-term effect.