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TNFSF14 (LIGHT) contributes to airway inflammation and remodelling. Here the authors show that TNFSF14 acting on its receptor TNFRSF14 on mast cells enhances their IgE-dependent activation and that interference with this pathway attenuates features of asthma pathology in mice.

Sarig and Tzahor et al. show that the multiple sclerosis drug glatiramer acetate improves cardiac function and reduces scar area in rodent models of acute myocardial infarction and ischemic heart failure.

A biodegradable pacemaker without external leads improves the safety of temporary cardiac pacing.

The role of outer mitochondrial membrane proteins in Myocardial Ischemia-reperfusion Injury (MIRI) largely remains unknown. Here, the authors demonstrate that the outer mitochondrial membrane protein Myocardial Mitochondrial Antiviral Signaling (MAVS) protein promotes MIRI suggesting MAVS protein as potential therapeutic target.

Monocytes participate in plaque formation, and adapt to metabolic changes to alter their functions. Here the authors show, using genetic mouse models and functional analyses, that Glut1-mediated glucose metabolism is important for regulating monocyte homeostasis and migration, but curiously has no impact on atherosclerotic plaque formation.

Here, the authors show that treatment with a monoclonal neutralizing antibody against the lung microbiota-derived proapoptotic peptide corisin ameliorates acute exacerbation of pulmonary fibrosis and severity of endotoxin-induced acute lung injury in mice.

Here, the authors investigate the proteome trajectory of human iPSCs differentiating into hepatic stellate cells (diHSCs) and identify RORA as a key transcription factor that governs metabolic reprogramming essential for diHSCs’ commitment, identity, and quiescent phenotype.

Critical regulators of RAS signaling pathways in oncogenic RAS-driven tumors remain to be explored. Here, the authors show the development of KRAS(G12D)-driven lung adenocarcinoma is dependent on SOS1, with dual roles in both tumor and stroma.

Individuals carrying a gain-of-function mutation in PKG1 develop thoracic aortic aneurysms and dissections. Here Schwaerzer et al. show that mice carrying the same mutation recapitulate the human disease, and find that treatment with anti-oxidants including cobinamide, a vitamin B12 analog, prevents disease progression.

The enzyme ACE2 is involved in cardiac pathology and can counteract heart failure and other cardio-pulmonary diseases. Here the authors show that bacteria produce an ACE2-like enzyme that is effective in suppressing cardiac hypertrophy and fibrosis in mice.

Alport syndrome is a progressive inherited nephritis accompanied by sensorineural loss of hearing and ocular abnormalities, for which there is currently no effective therapy. Here, the authors develop an exon-skipping therapy using an antisense-oligonucleotide and show it is effective in mouse models.

The so far reported enzyme mimics focus on the redox-active metal as a redox site, while the redox-inert metal as Lewis acid has so far not been reported. Here, the authors report efficient M_xV₂O₅·nH₂O peroxidase mimics with vanadium as redox site and alkaline-earth metal ion (M²⁺) as Lewis acid, where the peroxidase-mimicking activity shows a periodic change with the Lewis acidity of the metal.

A study reports whole-genome sequences for 490,640 participants from the UK Biobank and combines these data with phenotypic data to provide new insights into the relationship between human variation and sequence variation.

Kidney disease compromises the humoral immune response to vaccines and infections. Here authors show in multiple murine kidney disease models that apoptosis of germinal center B cells via hippuric-acid-driven loss of mitochondrial membrane potential is a central cause of diminished antibody response.

Short telomeres are risk factors for age-associated diseases such as cardiopathies. Here the authors show that cardiac reactivation of telomerase, the telomere-elongating enzyme whose expression is normally silenced postnatally, mitigates the consequences of myocardial infarction in adult mice.

Zhang et al. show that Egr1 regulates transient senescence during neonatal heart regeneration and upon agrin-mediated cardiac repair in adult mice, acting downstream of the integrin–FAK–ERK–Akt1 axis in cardiac fibroblasts.

Here, the authors develop a PMO-based heteroduplex oligonucleotide technology that enhances PMO delivery to tissues and normalizes motor/cardiac function and CNS symptoms in a mouse model of Duchenne muscular dystrophy.

The mechanisms and consequences of bioactive lipids release from lipid droplets remain poorly understood. Here the authors link a lipid droplet enzyme to mobilization of esters of regulatory sterols in foam cells and protection against atherosclerosis.

Scars are a significant problem caused by excess collagen in the skin. Here the authors develop a topical drug that reduces collagen stability and leads to improved scar appearance and stiffness in preclinical models.

A small molecule that mimics enhanced melanocortin 1 receptor signalling in response to ultraviolet light can stimulate pigmentation and thereby protect mice with light skin from DNA damage and cancer formation.

The advancement of upper tract urothelial carcinoma (UTUC) research is hampered by the lack of disease-specific models. Here, the authors report patient derived xenograft and cell line models of UTUC, and show that these models retain the genomic and biological heterogeneity of human disease.

Loss of the metalloproteinase Adamts1 leads to aortic pathology in mice due to increased NOS2-dependent NO production. Decreased Adamts1 expression, associated with increased NOS2 expression, occurs in Marfan syndrome (MFS) mice and in MFS patients, and NOS2 inhibition prevents and reverses aortic pathology in MFS mice.

Allergic asthma is one of the most common immune-mediated disorders. The authors investigated the possibility that TPRV4 cation channels facilitate the development of allergic asthma and subsequent pulmonary fibrosis in the lung. Their data suggest that TPRV4 is dispensable in the initiation and development of airway asthma and subsequent fibrosis.

Tzahor and colleagues show that ErbB2 signalling is required for cardiomyocyte proliferation in fetal and postnatal mouse hearts, and that its activation in adult hearts promotes cardiomyocyte proliferation and regeneration following myocardial ischaemic injury.

Therapeutic stress induces phenotypic plasticity in glioma stem cells although the mechanisms underlying this remain poorly understood. Here, the authors show that P300 mediates the radiation-induced vascular-like conversion of glioma stem cells to promote tumor recurrence.

Cardiac repair usually requires highly invasive interventional procedures. Here, the authors develop an injectable shape-memory cardiac patch and demonstrated its applicability in a myocardial infarction model.

The secreted factor follistatin-like 1 (FSTL1) becomes undetectable in the epicardium of infarcted hearts; when reconstituted using a collagen patch sutured onto an infarcted heart, FSTL1 can induce cell cycle entry and division of pre-existing cardiomyocytes, thus boosting heart function and survival in mouse and pig models of myocardial infarction.

Taylor et al. show that tumor cells promote white adipose tissue (WAT) wasting and cachexia by overactivation of Notch1 signaling and retinoic acid production in distant WAT endothelium, which can be therapeutically targeted to inhibit wasting.

The Bladder Cancer Advocacy Network established the UC-GENOME study in order to create a biobank and data repository for metastatic urothelial carcinoma. Here, the authors present the first characterization and analysis of DNA and RNA sequencing data from the 218 patients included in the UC-GENOME.

IgG4-related disease is a fibro-inflammatory disorder, characterized by infiltration of IgG4 producing plasma cells in the target organs. Here authors show that the affected B cells express less ubiquitin-specific protease 25 (USP25), and this results in activation of multiple pathways involved in cytoskeleton reorganization, inflammation and energy metabolism, which might govern disease pathogenesis.