Yingzi Liu, Antonella Tosti, Etienne C E Wang, Stefanie Heilmann-Heimbach, Crystal Aguh, Francisco Jimenez, Sung-Jan Lin, Ohsang Kwon, Maksim V Plikus
{"title":"Androgenetic alopecia.","authors":"Yingzi Liu, Antonella Tosti, Etienne C E Wang, Stefanie Heilmann-Heimbach, Crystal Aguh, Francisco Jimenez, Sung-Jan Lin, Ohsang Kwon, Maksim V Plikus","doi":"10.1038/s41572-025-00656-9","DOIUrl":"https://doi.org/10.1038/s41572-025-00656-9","url":null,"abstract":"<p><p>Androgenetic alopecia (AGA) is a condition of scalp hair growth characterized by progressive miniaturization of hair follicles and a reduction in the number of active follicles. In general, frontal, mid-scalp and crown hair follicles in postpubescent men and in postmenopausal women are susceptible to AGA. In rare cases, premenopausal women and prepubescent individuals are affected. In men, AGA is hypothesized to be caused by increased androgen signalling within susceptible hair follicles, altering the levels of locally produced signalling factors that sustain hair growth, whereas the molecular basis of AGA in women remains undetermined. AGA displays variability in its time of onset, severity and distribution patterns, and genome-wide association studies have uncovered more than 380 genomic loci associated with AGA, including genes involved in androgen and WNT pathways. Furthermore, epidemiological studies support substantial ancestral variation in AGA. Effective therapies for AGA include autologous transplantation of androgen-resistant occipital hair follicles, oral finasteride and topical minoxidil. Not all individuals with AGA respond to these therapies or comply with daily use of medicines, creating a need for new approaches. Emerging therapies for AGA include hair follicle-activating peptides, mRNA-containing liposomes, as well as bioengineering of new hair follicles. AGA has a negative socioemotional effect on affected individuals, and its prompt diagnosis and treatment can improve self-reported quality of life.</p>","PeriodicalId":18910,"journal":{"name":"Nature Reviews Disease Primers","volume":"11 1","pages":"73"},"PeriodicalIF":76.9,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145258547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Olivier Disson, Caroline Charlier, Philippe Pérot, Alexandre Leclercq, Ran Nir Paz, Sophia Kathariou, Yu-Huan Tsai, Marc Lecuit
{"title":"Listeriosis.","authors":"Olivier Disson, Caroline Charlier, Philippe Pérot, Alexandre Leclercq, Ran Nir Paz, Sophia Kathariou, Yu-Huan Tsai, Marc Lecuit","doi":"10.1038/s41572-025-00654-x","DOIUrl":"https://doi.org/10.1038/s41572-025-00654-x","url":null,"abstract":"<p><p>Listeriosis is a serious food-borne bacterial infection caused by Listeria monocytogenes. L. monocytogenes is a facultative intracellular bacterial species that can replicate inside human cells, as well as thrive in a variety of environments, including soil, decaying vegetation, animal intestines and foods such as unpasteurized dairy products, soft cheese, raw meat, fish, seafood, vegetables and fruits. Clinically, L. monocytogenes can cause gastroenteritis in healthy individuals or serious invasive infections in at-risk populations. For example, maternal-fetal infections during pregnancy can lead to adverse pregnancy outcomes. In the elderly and immunosuppressed, listeriosis can cause septicaemia and central nervous system infections (also known as neurolisteriosis) with high mortality and risk of long-term sequelae. Genomic studies have identified four lineages of L. monocytogenes, with lineage I comprising the most virulent strains. The pathogenicity of L. monocytogenes reflects its ability to resist gastric and bile acids, colonize the intestinal lumen, cross the intestinal barrier, survive intracellularly in the bloodstream, evade immune responses, and cross the placental and blood-brain barriers. Diagnosis of listeriosis (septicaemia, neurolisteriosis, maternal-neonatal listeriosis or focal listeriosis) involves clinical observations and microbiological testing based on bacterial culture or DNA detection in individuals with prior antimicrobial therapy. Treatment typically involves aminopenicillins and aminoglycosides, with no evidence of clinically meaningful acquired antimicrobial resistance. Although listeriosis is a well-studied infection, a clearer picture of its global burden, its pathophysiology, the dynamics of the L. monocytogenes population and transmission routes is needed. On the host side, new risk factors, including genetics, and new treatment regimens to improve patient outcomes need to be identified.</p>","PeriodicalId":18910,"journal":{"name":"Nature Reviews Disease Primers","volume":"11 1","pages":"71"},"PeriodicalIF":76.9,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ioannis Parodis, Brad H Rovin, Maria G Tektonidou, Hans-Joachim Anders, Ana Malvar, Chi Chiu Mok, Chandra Mohan
{"title":"Lupus nephritis.","authors":"Ioannis Parodis, Brad H Rovin, Maria G Tektonidou, Hans-Joachim Anders, Ana Malvar, Chi Chiu Mok, Chandra Mohan","doi":"10.1038/s41572-025-00653-y","DOIUrl":"https://doi.org/10.1038/s41572-025-00653-y","url":null,"abstract":"<p><p>Lupus nephritis (LN) is a type of glomerulonephritis and one of the most serious complications of systemic lupus erythematosus (SLE). LN affects 25-60% of patients with SLE, with incidence and prevalence varying by age, sex, ethnicity and socioeconomic factors. LN predominantly develops within 5 years of an SLE diagnosis and, for many patients, it is the initial manifestation that leads to the recognition of SLE. In some patients, LN may develop late in the disease course, highlighting the importance of persistent awareness of its symptoms and signs. Despite an increasing understanding of disease biology and more effective treatment options, LN remains a substantial cause of morbidity and mortality as it can lead to irreversible kidney failure and associated complications. Risk factors for progression to kidney failure include persistent proteinuria, low glomerular filtration rate, hypertension at diagnosis and frequent disease flares. LN pathogenesis involves complex immune dysregulation, with key pathways including type I interferon signalling, calcineurin activation, and B and T cell dysfunction. Several immunomodulatory drugs are used for the management of LN, and treatment paradigms are increasingly shifting towards multi-agent regimens. Along with appropriate pharmacotherapy, multidisciplinary care tailored to the patient's individual needs, involving rheumatologists, nephrologists, social workers and other health professionals, is crucial for holistically addressing both the immune and non-immune risk factors for progressive kidney function loss and for maximizing kidney lifespan in LN.</p>","PeriodicalId":18910,"journal":{"name":"Nature Reviews Disease Primers","volume":"11 1","pages":"69"},"PeriodicalIF":76.9,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Victor Aboyans, Mario Enrico Canonico, Lucie Chastaingt, Sonia S Anand, Marianne Brodmann, Thierry Couffinhal, Michael H Criqui, Eike Sebastian Debus, Lucia Mazzolai, Mary M McDermott, Marc P Bonaca
{"title":"Peripheral artery disease.","authors":"Victor Aboyans, Mario Enrico Canonico, Lucie Chastaingt, Sonia S Anand, Marianne Brodmann, Thierry Couffinhal, Michael H Criqui, Eike Sebastian Debus, Lucia Mazzolai, Mary M McDermott, Marc P Bonaca","doi":"10.1038/s41572-025-00651-0","DOIUrl":"https://doi.org/10.1038/s41572-025-00651-0","url":null,"abstract":"<p><p>Peripheral artery disease (PAD) is characterized by blockage of the arteries that supply the lower extremities, often occurring as a result of atherosclerosis and thrombosis. PAD affects approximately 230 million people worldwide, with a growing prevalence owing to population ageing and concomitant cardiovascular risk factors, including smoking, diabetes mellitus, hypertension and dyslipidaemia. Patients with PAD have an increased risk of major cardiovascular and limb events, and substantially poorer walking performance compared with those without PAD. The screening and identification of PAD involves clinical and imaging assessments of disease extent and severity and stratification of individual risk to ensure appropriate management. Patients with PAD should be treated with guideline-directed medical therapy (GDMT), including antithrombotic, lipid-lowering, glucose-lowering and anti-hypertensive therapies, and exercise therapies that aim to improve function as well as cardiovascular and limb outcomes. For patients with compromised limb viability, such as acute and chronic limb-threatening ischaemia, or severe functional impairment that does not improve with exercise training, lower extremity revascularization is recommended. Given the complexity of PAD management, a multidisciplinary vascular team is required to achieve the best individualized treatment. Further research efforts should focus on reducing ischaemic events and health disparities and on optimizing the implementation of GDMT and exercise therapy, as well as improving the quality of life in patients with PAD.</p>","PeriodicalId":18910,"journal":{"name":"Nature Reviews Disease Primers","volume":"11 1","pages":"68"},"PeriodicalIF":76.9,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marienke A A M de Bruijn, Frank Leypoldt, Josep Dalmau, Soon-Tae Lee, Jerome Honnorat, Stacey L Clardy, Sarosh R Irani, Ava Easton, Amy Kunchok, Maarten J Titulaer
{"title":"Autoimmune encephalitis.","authors":"Marienke A A M de Bruijn, Frank Leypoldt, Josep Dalmau, Soon-Tae Lee, Jerome Honnorat, Stacey L Clardy, Sarosh R Irani, Ava Easton, Amy Kunchok, Maarten J Titulaer","doi":"10.1038/s41572-025-00650-1","DOIUrl":"10.1038/s41572-025-00650-1","url":null,"abstract":"<p><p>Autoimmune encephalitis (AE) is a treatable neuro-inflammatory disorder that is increasing in incidence. AE can be associated with malignancy (paraneoplastic), but in many patients no tumour is present. The disease presentation of AE can be heterogeneous depending on the type of antibody involved. AE is often caused by neuronal antibodies that bind to extracellular autoantigens (that is, N-methyl-D-aspartate receptor (NMDAR) and LGI1). Binding of these antibodies causes dysfunction of synaptic receptors, which leads to neurological symptoms. In these patients, treatment with immunosuppressive therapies is believed to decrease inflammation and deplete antibodies, and is essential for recovery. AE can also occur in patients with antibodies against intracellular antigens (such as Hu and Ri), often in the setting of malignancy. In these patients, tumour treatment is essential for stabilization or improvement. The most frequent symptoms of AE are cognitive problems, behavioural changes and seizures. Rapid recognition of AE syndromes is essential as earlier treatment of AE leads to better outcomes. For a definite diagnosis, the identification of an autoantibody is essential; however, some patients have seronegative AE. Most patients are severely affected during the acute disease stage, but long-term functional recovery is often good, particularly for patients without cancer. Nevertheless, residual anxiety, fatigue and cognitive problems can considerably affect quality of life. Research focuses on improving the understanding of pathophysiological processes, establishing patient-tailored outcome measures, optimizing treatment prediction models and studying different therapeutic regimens, all aiming to improve treatment and long-term outcomes.</p>","PeriodicalId":18910,"journal":{"name":"Nature Reviews Disease Primers","volume":"11 1","pages":"65"},"PeriodicalIF":76.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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