Reabsorption of iron into acutely damaged rat liver:A role for ferritins

AIM To studied iron metabolism in liver, spleen, and serum after acute liver-damage, in relation to surrogate markers for liver-damage and repair.METHODS Rats received intraperitoneal injection of the hepatotoxin thioacetamide(TAA), and were sacrificed regularly between 1 and 96 h thereafter. Serum levels of transaminases and iron were measured using conventional laboratory assays. Liver tissue was used for conventional histology, immunohistology, and iron staining. The expression of acute-phase cytokines, ferritin light chain(FTL), and ferritin heavy chain(FTH)was investigated in the liver by q RT-PCR. Western blotting was used to investigate FTL and FTH in liver tissue and serum. Liver and spleen tissue was also used to determine iron concentrations.RESULTS After a short initial decrease, iron serum concentrations increased in parallel with serum transaminase(aspartate aminotransferase and alanine aminotransferase) levels, which reached a maximum at 48 h, and decreased thereafter. Similarly, after 48 h a significant increase in FTL, and after 72 h in FTH was detected in serum. While earliest morphological signs of inflammation in liver were visible after 6 h, increased expression of the two acute-phase cytokines IFN-γ(1 h) and IL-1β(3 h) was detectable earlier, with maximum values after 12-24 h. Iron concentrations in liver tissue increased steadily between 1 h and 48 h, and remained high at 96 h. In contrast, spleen iron concentrations remained unchanged until 48 h, and increased mildly thereafter(96 h). Although tissue iron staining was negative, hepatic FTL and FTH protein levels were strongly elevated. Our results reveal effects on hepatic iron concentrations after direct liver injury by TAA. The increase of liver iron concentrations may be due to the uptake of a significant proportion of the metal by healthy hepatocytes, and only to a minor extent by macrophages, as spleen iron concentrations do not increase in parallel. The temporary increase of iron, FTH and transaminases in serum is obviously due to their release by damaged hepatocytes.CONCLUSION Increased liver iron levels may be the consequence of hepatocyte damage. Iron released into serum by damaged hepatocytes is obviously transported back and stored via ferritins.

Fecal cytolysin does not predict disease severity in acutely decompensated cirrhosis and acute-on-chronic liver failure

Background:Cirrhosis with acute decompensation(AD)and acute-on-chronic liver failure(ACLF)are characterized by high morbidity and mortality.Cytolysin,a toxin from Enterococcus faecalis(E.faecalis),is associated with mortality in alcohol-associated hepatitis(AH).It is unclear whether cytolysin also contributes to disease severity in AD and ACLF.Methods:We studied the role of fecal cytolysin in 78 cirrhotic patients with AD/ACLF.Bacterial DNA from fecal samples was extracted and real-time quantitative polymerase chain reaction(PCR)was performed.The association between fecal cytolysin and liver disease severity in cirrhosis with AD or ACLF was analyzed.Results:Fecal cytolysin and E.faecalis abundance did not predict chronic liver failure(CLIF-C)AD and ACLF scores.Presence of fecal cytolysin was not associated with other liver disease markers,including Fibrosis-4(FIB-4)index,‘Age,serum Bilirubin,INR,and serum Creatinine(ABIC)’score,Child-Pugh score,model for end-stage liver disease(MELD)nor MELD-Na scores in AD or ACLF patients.Conclusions:Fecal cytolysin does not predict disease severity in AD and ACLF patients.The predictive value of fecal cytolysin positivity for mortality appears to be restricted to AH.

Comparing role of ATP between acute pain in neuromyelitis optica spectrum disorder and peripheral neuropathic pain

In this article, we present our previous research, which highlighted adenosine triphosphate(ATP) as the cause of neuropathic pain during the acute phase of neuromyelitis optica spectrum disorder(NMOSD). In NMOSD pathology, damageassociated molecular patterns(DAMPs), including ATP, are released from damaged astrocytes, triggering the activation of innate immune cells. ATP is a central mediator of acute pain in NMOSD.

Dip2a regulates stress susceptibility in the basolateral amygdala

Dysregulation of neurotransmitter metabolism in the central nervous system contributes to mood disorders such as depression, anxiety, and post–traumatic stress disorder. Monoamines and amino acids are important types of neurotransmitters. Our previous results have shown that disco-interacting protein 2 homolog A(Dip2a) knockout mice exhibit brain development disorders and abnormal amino acid metabolism in serum. This suggests that DIP2A is involved in the metabolism of amino acid–associated neurotransmitters. Therefore, we performed targeted neurotransmitter metabolomics analysis and found that Dip2a deficiency caused abnormal metabolism of tryptophan and thyroxine in the basolateral amygdala and medial prefrontal cortex. In addition, acute restraint stress induced a decrease in 5-hydroxytryptamine in the basolateral amygdala. Additionally, Dip2a was abundantly expressed in excitatory neurons of the basolateral amygdala, and deletion of Dip2a in these neurons resulted in hopelessness-like behavior in the tail suspension test. Altogether, these findings demonstrate that DIP2A in the basolateral amygdala may be involved in the regulation of stress susceptibility. This provides critical evidence implicating a role of DIP2A in affective disorders.

Vagus nerve stimulation in intracerebral hemorrhage:the need for further research

Vagus nerve stimulation(VNS)and stroke:Stroke is the second leading cause of death and the third leading cause of disability worldwide(Baig et al.,2023).There have been significant paradigm shifts in the management of acute ischemic stroke through mechanical thrombectomy.In chronic ischemic stroke,invasive VNS paired with rehabilitation is associated with a significant increase in upper limb motor recovery and is FDA-approved(Baig et al.,2023).There are no treatments of similar efficacy in acute intracerebral hemorrhage(ICH)where several promising trials,e.g.,TICH-2,STOP-AUST,and TRAIGE did not show improvements in functional outcomes(Puy et al.,2023).

Successful emergency surgical intervention in acute non-STsegment elevation myocardial infarction with rupture:A case report

BACKGROUND The incidence of acute myocardial infarction(AMI)is rising,with cardiac rupture accounting for approximately 2%of deaths in patients with acute ST-segment elevation myocardial infarction(STEMI).Ventricular free wall rupture(FWR)occurs in approximately 2%of AMI patients and is notably rare in patients with non-STEMI.Types of cardiac rupture include left ventricular FWR,ventricular septal rupture,and papillary muscle rupture.The FWR usually leads to acute cardiac tamponade or electromechanical dissociation,where standard resuscitation efforts may not be effective.Ventricular septal rupture and papillary muscle rupture often result in refractory heart failure,with mortality rates over 50%,even with surgical or percutaneous repair options.CASE SUMMARY We present a rare case of an acute non-STEMI patient who suffered sudden FWR causing cardiac tamponade and loss of consciousness immediate before undergoing coronary angiography.Prompt resuscitation and emergency open-heart repair along with coronary artery bypass grafting resulted in successful patient recovery.CONCLUSION This case emphasizes the risks of AMI complications,shares a successful treatment scenario,and discusses measures to prevent such complications.

Non-coding RNAs in acute ischemic stroke:from brain to periphery

Acute ischemic stroke is a clinical emergency and a condition with high morbidity,mortality,and disability.Accurate predictive,diagnostic,and prognostic biomarkers and effective therapeutic targets for acute ischemic stroke remain undetermined.With innovations in high-throughput gene sequencing analysis,many aberrantly expressed non-coding RNAs(ncRNAs)in the brain and peripheral blood after acute ischemic stroke have been found in clinical samples and experimental models.Differentially expressed ncRNAs in the post-stroke brain were demonstrated to play vital roles in pathological processes,leading to neuroprotection or deterioration,thus ncRNAs can serve as therapeutic targets in acute ischemic stroke.Moreover,distinctly expressed ncRNAs in the peripheral blood can be used as biomarkers for acute ischemic stroke prediction,diagnosis,and prognosis.In particular,ncRNAs in peripheral immune cells were recently shown to be involved in the peripheral and brain immune response after acute ischemic stroke.In this review,we consolidate the latest progress of research into the roles of ncRNAs(microRNAs,long ncRNAs,and circular RNAs)in the pathological processes of acute ischemic stroke–induced brain damage,as well as the potential of these ncRNAs to act as biomarkers for acute ischemic stroke prediction,diagnosis,and prognosis.Findings from this review will provide novel ideas for the clinical application of ncRNAs in acute ischemic stroke.

Persistent alterations in gray matter in COVID-19 patients experiencing sleep disturbances:a 3-month longitudinal study

Sleep disturbances are among the most prevalent neuropsychiatric symptoms in individuals who have recovered from severe acute respiratory syndrome coronavirus 2 infections.Previous studies have demonstrated abnormal brain structures in patients with sleep disturbances who have recovered from coronavirus disease 2019(COVID-19).However,neuroimaging studies on sleep disturbances caused by COVID-19 are scarce,and existing studies have primarily focused on the long-term effects of the virus,with minimal acute phase data.As a result,little is known about the pathophysiology of sleep disturbances in the acute phase of COVID-19.To address this issue,we designed a longitudinal study to investigate whether alterations in brain structure occur during the acute phase of infection,and verified the results using 3-month follow-up data.A total of 26 COVID-19 patients with sleep disturbances(aged 51.5±13.57 years,8 women and 18 men),27 COVID-19 patients without sleep disturbances(aged 47.33±15.98 years,9 women and 18 men),and 31 age-and gender-matched healthy controls(aged 49.19±17.51 years,9 women and 22 men)were included in this study.Eleven COVID-19 patients with sleep disturbances were included in a longitudinal analysis.We found that COVID-19 patients with sleep disturbances exhibited brain structural changes in almost all brain lobes.The cortical thicknesses of the left pars opercularis and left precuneus were significantly negatively correlated with Pittsburgh Sleep Quality Index scores.Additionally,we observed changes in the volume of the hippocampus and its subfield regions in COVID-19 patients compared with the healthy controls.The 3-month follow-up data revealed indices of altered cerebral structure(cortical thickness,cortical grey matter volume,and cortical surface area)in the frontal-parietal cortex compared with the baseline in COVID-19 patients with sleep disturbances.Our findings indicate that the sleep disturbances patients had altered morphology in the cortical and hippocampal structures during the acute phase of infection and persistent changes in cortical regions at 3 months post-infection.These data improve our understanding of the pathophysiology of sleep disturbances caused by COVID-19.

Hepatorenal syndrome:Paving a pathway from a fatal condition to an opportunity to preserve kidney function

In the 19^(th)century,von Frerichs F and Flint A identified a type of acute renal impairment associated with advanced liver disease,characterized by oliguria,absence of proteinuria,and normal renal histology,which was later termed hepatorenal syndrome(HRS).HRS primarily affects cirrhotic patients with ascites and often follows severe infections,digestive hemorrhages,or high-volume paracentesis.Pathophysiologically,HRS involves low glomerular filtration rate,hypotension,renin-angiotensin axis activation,water clearance,hyponatremia,and minimal urinary sodium excretion.These conditions mimic those seen in decreased effective circulatory volume(ECV)scenarios such as septic shock or heart failure.HRS represents a specific form of prerenal acute kidney injury(AKI)in patients with baseline renal ischemia,where the kidney attempts to correct decreased ECV by retaining sodium and water.Intense renal vasoconstriction,passive hyperemia from ascites,and acute tubular necrosis(ATN)with specific urinary sediment changes are observed.Persistent oliguria may transition HRS to ATN,although this shift is less straightforward than in other prerenal AKI contexts.Notably,liver grafts from HRS patients can recover function more rapidly than those from other ischemic conditions.Experimental studies,such as those by Duailibe et al,using omega-3 fatty acids in cirrhotic rat models,have shown promising results in reducing oxidative stress and improving kidney function.These findings suggest potential therapeutic strategies and underscore the need for further research to understand the mechanisms of HRS and explore possible treatments.Future research should address the impact of omega-3 on survival and secondary outcomes,as well as consider the balance of therapeutic risks and benefits in severe liver disease.

Persistent challenges in the diagnosis of acute pancreatitis due to primary hyperparathyroidism during pregnancy

In this manuscript,we provide critical commentary on the systematic review by Augustin et al,which investigated acute pancreatitis induced by primary hyperparathyroidism during pregnancy.Although this is an infrequent complication,it poses severe risks to both maternal and fetal health.Due to its infrequent occurrence in clinical practice,this review is based on an analysis of individual case reports over the past 55 years.While this is not the first study to utilize this sampling method for primary hyperparathyroidism-induced acute pancreatitis,it is unique in that it has a sufficiently large sample size with statistically significant results.Our discussion focuses on the diagnostic challenges associated with this condition,which are grounded in the mechanisms of parathyroid hormone secretion and variations in serum calcium levels.We also address the limitations of the current review and suggest potential strategies to increase diagnostic accuracy and improve health outcomes for both mothers and fetuses during pregnancy.

Bivalirudin for anticoagulation in elderly acute coronary syndrome:Effects on myocardial microcirculation and adverse events

The management of acute coronary syndrome(ACS)in older patients remains challenging because standard anticoagulants often fail to yield optimal outcomes.Bivalirudin,a direct inhibitor of thrombin,serves as an alternative to traditional therapies.This drug is particularly effective in enhancing myocardial microcircu-lation and reducing adverse events after clinical interventions.The present article explores the findings of a recent study that highlighted the clinical benefits of bivalirudin by investigating its effects on myocardial microcirculation and adverse cardiac events after percutaneous coronary intervention in older patients with ACS.Compared with unfractionated heparin,bivalirudin markedly reduced the emergency response time and improved cardiac function indicators.It further mitigated the risks of cardiovascular events and recurrent myocardial infarctions.These findings suggest that bivalirudin can enhance myocardial perfusion and reduce bleeding complications,thus serving as a safe,effective anticoagulation agent for older patients with ACS.Nonetheless,further large-scale,high-quality trials are needed to establish optimal usage guidelines and assess long-term outcomes.Integrating bivalirudin into ACS treatment protocols for older patients may help optimize patient care,balancing efficacy and safety.Continual research and consensus building are necessary for the widespread clinical application of bivalirudin and the improvement of ACS outcomes in older patients.

Acute abdominal pain complicated by cecal perforation caused by an unnoticed swallowed toothpick:A case report

BACKGROUND Acute abdominal pain is one of the most common gastrointestinal symptoms.The etiology of acute abdomen can be challenging for gastroenterologists to establish.Cecal foreign body is a rare cause of cecal perforation.CASE SUMMARY We report a 35-year-old male from China who initially exhibited symptoms suggestive of acute appendicitis.However,during a minimally invasive colonoscopy procedure,the authors found that a wooden toothpick caused the perforation.The patient presented to our emergency department with a 2 days history of right lower abdominal pain and low grade fever.The patient was in good health and had eaten fish 2 days earlier.Physical examination revealed mild pain with positive rebound tenderness in the right lower abdomen.However,computed tomography of the abdomen confirmed a strip of high-density shadows protruding beyond the intestinal cavity outline,with a small amount of peritoneal seepage in the ileocecal area.Combined with the medical history,the possibility of foreign body perforation by a fishbone and peripheral peritonitis were considered.However,the high-density shadow was identified as a wooden toothpick,which was removed via a minimally invasive procedure using a foreign body forceps under colonoscopy.The patient's condition improved significantly within 5 days after treatment.CONCLUSION We emphasize the importance of a detailed patient history,accurate diagnosis and proper treatment in patients with acute abdomen.

Transition from acute kidney injury to chronic kidney disease in liver cirrhosis patients:Current perspective

In liver cirrhosis patients,acute kidney injury(AKI)is a common and severe complication associated with significant morbidity and mortality,often leading to chronic kidney disease(CKD).This progression reflects a complex interplay of renal and hepatic pathophysiology,with AKI acting as an initiator through maladaptive repair mechanisms.These mechanisms—such as tubular cell cycle arrest,inflammatory cascades,and fibrotic processes—are exacerbated by the hemodynamic and neurohormonal disturbances characteristic of cirrhosis.Following AKI episodes,persistent kidney dysfunction or acute kidney disease(AKD)often serves as a bridge to CKD.AKD represents a critical phase in renal deterioration,characterized by prolonged kidney injury that does not fully meet CKD criteria but exceeds the temporal scope of AKI.The progression from AKD to CKD is further influenced by recurrent AKI episodes,impaired renal autoregu-lation,and systemic comorbidities such as diabetes and metabolic dysfunction-associated steatotic liver disease,which compound kidney damage.The clinical management of AKI and CKD in cirrhotic patients requires a multidimensional approach that includes early identification of kidney injury,the application of novel biomarkers,and precision interventions.Recent evidence underscores the inadequacy of traditional biomarkers in predicting the AKI-to-CKD progression,necessitating novel biomarkers for early detection and intervention.

Prevalence of RUNX1 gene alterations in de novo adult acute myeloid leukemia

BACKGROUND Acute myeloid leukemia(AML)is a complicated disease with uncontrolled hematopoietic precursor proliferation induced by various genetic alterations.Runt-related transcription factor-1(RUNX1)is commonly disrupted by chromosomal translocations in hematological malignancies.AIM To characterize RUNX1 gene rearrangements and copy number variations in newly diagnosed adult AML patients,with an emphasis on the impact of clinical and laboratory features on the outcome.METHODS Fluorescence in situ hybridization was used to test RUNX1 gene alterations in 77 newly diagnosed adult AML cases.NPM1,FLT3/ITD,FLT3/TKD,and KIT mutations were tested by PCR.Prognostic clinical and laboratory findings were studied in relation to RUNX1 alterations.RESULTS RUNX1 abnormalities were detected by fluorescence in situ hybridization in 41.6%of patients:20.8%had translocations,22.1%had amplification,and 5.2%had deletion.Translocations prevailed in AML-M2(P=0.019)with a positive expression of myeloperoxidase(P=0.031),whereas deletions dominated in M4 and M5 subtypes(P=0.008)with a positive association with CD64 expression(P=0.05).The modal chromosomal number was higher in cases having amplifications(P=0.007)and lower in those with deletions(P=0.008).RUNX1 abnormalities were associated with complex karyotypes(P<0.001)and were mutually exclusive of NPM1 mutations.After 44 months of follow-up,RUNX1 abnormalities affected neither patients’response to treatment nor overall survival.CONCLUSION RUNX1 abnormalities were mutually exclusive of NPM1 mutations.RUNX1 abnormalities affected neither patients’response to treatment nor overall survival.

Neutrophil gelatinase-associated lipocalin as a biomarker for neuropsychiatric complications in acute ischemic stroke

This study evaluates the findings of Gu et al,who investigated the role of neutrophil gelatinase-associated lipocalin(NGAL)as a biomarker for predicting neuropsychiatric complications in acute ischemic stroke(AIS)patients.The results revealed that elevated serum NGAL levels at admission are associated with a higher risk of cognitive impairment,anxiety,and depressive symptoms at discharge.The study analyzed 150 AIS patients(mean age 65.4 years,58%male)using the Mini-Mental State Examination and the Hospital Anxiety and Depression Scale to assess neuropsychiatric outcomes.Multivariate analysis demonstrated that higher NGAL levels were independent predictors of cognitive impairment[odds ratio(OR)=1.42],anxiety(OR=1.28),and depression(OR=1.39).Notably,NGAL exhibited strong predictive power for cognitive impairment,with an area under the curve of 0.78.Despite these promising findings,NGAL’s clinical utility is limited by its non-specificity across various conditions.Nevertheless,NGAL levels could help identify AIS patients at risk for neuropsychiatric complications,enabling timely intervention and comprehensive neuropsychiatric evaluation.The study emphasizes the need for further research to validate NGAL’s predictive accuracy and specificity in diverse AIS populations and advocates for its integration with other diagnostic modalities to enhance clinical decision-making.

Link between obstructive uropathy and acute kidney injury

Obstructive uropathy represents a major risk of acute kidney injury.From an epidemiological point of view,it is responsible for 5%to 10%of cases of acute renal failure and 4%of cases of end-stage kidney disease.Although obstructive uropathy is a recognized disease,there is a significant lack of detailed research on this topic from both a nephrological and urological perspective.The majority of published research focuses on the pathophysiology of the topic and neglects a comprehensive analysis of diagnostic and treatment approaches supported by current data.In this context,it is crucial to assess the overall hemodynamic status,especially in the presence of urosepsis.Once clinical stability is assured,it is important to focus on symptom management,usually by controlling pain.Ultimately,it is crucial to decide immediately whether the patient should receive a prompt urinary diversion.Urinary diversion is an essential part of the treatment of obstructive uropathy and should be initiated promptly and without unnece-ssary delay once the diagnosis has been confirmed.Functional recovery of the obstructed kidney after decompression of the urinary tract depends on the degree of obstruction,the duration of the obstruction and the presence of a concomitant urinary tract infection.The timing and proper treatment of this condition determines the recovery of kidney function after an obstruction and prevents the development of chronic kidney disease.In this editorial,we emphasized the pathophysiological role and clinical significance of obstructive uropathy in the context of acute kidney injury.

Pegaspargase induced multiple organ failure with acute lymphoblastic leukemia:A case report

BACKGROUND The introduction of pegaspargase has greatly advanced the treatment of acute lymphoblastic leukemia(ALL).In the literature,only one case of pegaspargaseinduced multiple organ failure has been reported,and the patient died due to multiple organ failure.CASE SUMMARY Herein,we present a rare case of a 40-year-old man with ALL who developed multiple organ failure after treatment with pegaspargase.The patient had two rare phenomena reflecting poor prognosis,including the discrepancy between clinical manifestations and liver function and persistently low alpha-fetoprotein(AFP)levels from subacute liver failure.However,the patient was successfully treated using a multidisciplinary team approach.CONCLUSION This is the first case report of successful treatment of pegaspargase-induced multiple organ failure.The findings emphasize the importance of a multidisciplinary team approach in treating pegaspargase-induced multiple organ failure.

Protective effects of autologous bone marrow-derived mesenchymal stem cell transplantation on acute radioactive enteritis in Beagle dogs

BACKGROUND Radiation enteritis is a common complication of radiation therapy in which the surrounding normal intestinal tissue is damaged by ionising radiation,and there is no standard pharmacological prophylaxis or treatment regimen available.Mesenchymal stem cell transplantation can be used for radiation protection and the treatment of acute radiation injury,but its therapeutic mechanism of action remains unclear.AIM To investigate the protective effects of autologous bone marrow-derived mesenchymal stem cell(ABMSC)transplantation on radiation-induced intestinal injury.METHODS A model of acute radioactive enteritis was established in dogs by applying abdominal intensity-modulated radiation at a single X-ray dose of 12 Gy.ABMSCs were transplanted into the mesenteric artery with the technology of femoral artery puncture and DSA imaging two days after radiation.Visual and histopathological changes of the experimental dogs were observed.Different kinds of cytokines from intestinal samples were tested using Quantibody Canine Cytokine Array method.Enzyme-linked immunosorbent assay(ELISA)was also used to evaluate the cytokines changes in serum.RESULTS The ABMSCs group showed significant improvements in survival status compared with the blank and saline treatment groups.Histological observations revealed that the former had lower histological scores than the later after treatment(P<0.05).Compared to the control groups,interleukin(IL)-10 and monocyte chemotactic protein(MCP)-1 from intestinal samples showed a remarkable increase and ELISA of serum samples proved higher secretion of the two target cytokines in the ABMSCs group(P<0.05).CONCLUSION Our data suggest that transplantation of ABMSCs promotes intestinal recovery after acute radioactive injury in Beagle dogs.The cytokines of IL-10 and MCP-1 might play an important role in this process.

Functional metabolomics analysis of the protective mechanism of total flavonoids of Scutellaria baicalensis on acute myocardial ischemia rats

Background:The study aimed to investigate the protective effect and mechanism of total flavonoids of Scutellaria baicalensis(TFSB)on acute myocardial ischemia(AMI)rats by using functional metabonomics.Methods:Rats were divided into the Control,Model,AMI positive control(Propranolol hydrochloride,30 mg/kg),low dose TFSB(50 mg/kg),and high dose TFSB(100 mg/kg)groups.Rats received the corresponding treatment by intragastric administration once daily for 10 consecutive days.Electrocardiogram,myocardial enzyme,triphenyltetrazolium chloride staining,hematoxylin-eosin,and enzyme-linked immunosorbent assay were performed to evaluate the protective effect of TFSB on AMI rats.Then,the UHPLC-Q-Orbitrap MS method based on serum metabolomics was utilised to search for metabolic biomarkers and metabolic pathways.Subsequently,Western blot and RT-PCR techniques were employed to identify the respective genes and proteins.Results:Pharmacodynamics revealed that TFSB could ameliorate AMI in rats.The results of the metabolomics analysis indicated that the alterations in metabolic profile observed in rats with AMI were partially improved by treatment with TFSB.Moreover,the mRNA expression levels of 5-lipoxygenase(5-LOX)and 15-lipoxygenase(15-LOX)and the protein expression levels of 5-LOX,15-LOX,interleukin-1β(IL-1β),and NF-κB p65 were reduced following treatment with TFSB.Conclusion:The potential treatment of TFSB in AMI may be ascribed to its ability to regulate arachidonic acid metabolism.

Exploring the mechanistic role of epidermal growth factor receptor activation in non-cancer kidney disease

The epidermal growth factor receptor(EGFR)is a transmembrane glycoprotein that plays a crucial role in signal transduction and cellular responses.This review explores the function of EGFR in kidney physiology and its implications for various kidney diseases.EGFR signaling is essential for kidney function and repair mechanisms,and its dysregulation significantly impacts both acute and chronic kidney conditions.The review discusses the normal distribution of EGFR in kidney tubular segments,the mechanism of its activation and inhibition,and the therapeutic potential of EGFR-targeting antagonists and ligands.Additionally,it explores the pathophysiological characteristics observed in rodent models of kidney diseases through pharmacological and genetic inhibition of EGFR,highlighting therapeutic challenges and limitations such as species differences,variability in disease models,and potential adverse effects.Overall,the findings underscore the multifaceted role of EGFR in kidney diseases,influencing inflammation,fibrosis,and tissue injury.This complex involvement suggests that targeting EGFR may be a beneficial therapeutic strategy for managing these conditions,potentially mitigating inflammation and fibrosis while promoting tissue repair.