TY - JOUR AU - Blaas, L.* AU - Matta Pereira, L. C1 - 75256 C2 - 57909 CY - 111 River St, Hoboken 07030-5774, Nj Usa TI - SAF-guarding the cuff: Could shoulder fat cells combat fibrosis? JO - J. Physiol.-London PB - Wiley PY - 2025 SN - 0022-3751 ER - TY - JOUR AU - Matta Pereira, L. AU - Blaas, L.* AU - Gibis, C.* AU - Garcia Guerra, J.F. C1 - 70395 C2 - 55602 CY - 111 River St, Hoboken 07030-5774, Nj Usa TI - Functions require junctions: Endurance exercise protects from age-induced alterations of the neuromuscular system. JO - J. Physiol.-London PB - Wiley PY - 2024 SN - 0022-3751 ER - TY - JOUR AU - Wackerhage, H.* AU - Hinrichs, A.* AU - Wolf, E.* AU - Hrabě de Angelis, M. C1 - 70096 C2 - 55418 CY - 111 River St, Hoboken 07030-5774, Nj Usa SP - 1655-1658 TI - Turning fat into muscle: can this be an alternative to anti-obesity drugs such as semaglutide? JO - J. Physiol.-London VL - 602 IS - 8 PB - Wiley PY - 2024 SN - 0022-3751 ER - TY - JOUR AU - Matta Pereira, L. AU - Blaas, L.* AU - de Faria, C.C.* C1 - 67171 C2 - 54230 CY - 111 River St, Hoboken 07030-5774, Nj Usa SP - 711-713 TI - From honeymoon to dysfunction: Brown fat remodeling in obesity. JO - J. Physiol.-London VL - 601 IS - 4 PB - Wiley PY - 2023 SN - 0022-3751 ER - TY - JOUR AB - Nonalcoholic fatty liver disease (NAFLD), recently re-named to metabolic dysfunction associated fatty liver disease (MAFLD) is a major health problem, as it affects ∼25% of the population globally and is a major cause of hepatic cirrhosis and thereby liver failure, as well as hepatocellular carcinoma (HCC). MALFD comprises a broad range of pathological conditions in the liver, including simple fat accumulation (steatosis) and the more progressive non-alcoholic steatohepatitis (NASH) that can lead to fibrosis development. Cells of innate immunity, and particularly macrophages, comprising the liver resident Kupffer cells and the recruited monocyte-derived macrophages play complex roles in NASH-related inflammation and disease progression to fibrosis. Here, we discuss the recent developments with regards to the function of liver macrophage subpopulations during MAFLD development and progression. Abstract figure legend: Liver macrophages in metabolic dysfunction associated fatty liver disease. Different liver macrophage subpopulations, including Kupffer cells (KC) and monocyte-derived macrophages (MoMf), play multiple roles in the pathogenesis and progression of metabolic dysfunction associated fatty liver disease (MAFLD). This article is protected by copyright. All rights reserved. AU - Subramanian, P.* AU - Chavakis, T. C1 - 67534 C2 - 54097 CY - 111 River St, Hoboken 07030-5774, Nj Usa SP - 1159-1171 TI - The complex function of macrophages and their subpopulations in metabolic injury associated fatty liver disease. JO - J. Physiol.-London VL - 601 IS - 7 PB - Wiley PY - 2023 SN - 0022-3751 ER - TY - JOUR AB - KEY POINTS: Obesity and the associated adipocyte pathology are risk factors for cardiovascular disease Translational research is possible but strongly depends on the mouse model used White adipose tissue inflammation contributes to metabolic and vascular dysfunction Brown adipose tissue thermogenesis supports metabolic and vascular function ABSTRACT: Obesity is a medical disorder caused by multiple mechanisms of dysregulated energy balance. A major consequence of obesity is an increased risk to develop diabetes, diabetic complications, and cardiovascular disease. While a better understanding of the molecular mechanisms linking obesity, insulin resistance, and cardiovascular disease is needed, translational research of the human pathology is hampered by the available cellular and rodent model systems. Major barriers are the species-specific differences in energy balance, vascular biology, and adipose tissue physiology, especially related to white and brown adipocytes, and adipose tissue browning. In rodents, non-shivering thermogenesis is responsible for a large part of energy expenditure, but humans possess much less thermogenic fat, which makes temperature is an important variable in translational research. Mouse models with predisposition to dyslipidaemia housed at thermoneutrality and fed a high-fat diet more closely reflect human physiology. Also, adipocytes play a key role in the endocrine regulation of cardiovascular function. Adipocytes secrete a variety of hormones, lipid mediators, and other metabolites that directly influence the local microenvironment as well as distant tissues. This is specifically apparent in perivascular depots, where adipocytes modulate vascular function and inflammation. Altogether, these mechanisms highlight the critical role of adipocytes in the development of cardiometabolic disease. Abstract figure legend While cardiometabolic health is associated with adipose tissue browning and beneficial adipokine profiles, obesity leads to adipose tissue whitening, inflammation, and atherosclerosis. This article is protected by copyright. All rights reserved. AU - Giroud, M. AU - Jodeleit, H.* AU - Prentice, K.J.* AU - Bartelt, A. C1 - 63119 C2 - 51330 CY - 111 River St, Hoboken 07030-5774, Nj Usa TI - Adipocyte function and the development of cardiometabolic disease. JO - J. Physiol.-London PB - Wiley PY - 2021 SN - 0022-3751 ER - TY - JOUR AB - Key points: Muscular dystrophy patients suffer from progressive degeneration of skeletal muscle fibres, sudden spontaneous falls, balance problems, as well as gait and posture abnormalities. Dystrophin- and dysferlin-deficient mice, models for different types of muscular dystrophy with different aetiology and molecular basis, were characterized to investigate if muscle spindle structure and function are impaired. The number and morphology of muscle spindles were unaltered in both dystrophic mouse lines but muscle spindle resting discharge and their responses to stretch were altered. In dystrophin-deficient muscle spindles, the expression of the paralogue utrophin was substantially upregulated, potentially compensating for the dystrophin deficiency. The results suggest that muscle spindles might contribute to the motor problems observed in patients with muscular dystrophy. Abstract: Muscular dystrophies comprise a heterogeneous group of hereditary diseases characterized by progressive degeneration of extrafusal muscle fibres as well as unstable gait and frequent falls. To investigate if muscle spindle function is impaired, we analysed their number, morphology and function in wildtype mice and in murine model systems for two distinct types of muscular dystrophy with very different disease aetiology, i.e. dystrophin- and dysferlin-deficient mice. The total number and the overall structure of muscle spindles in soleus muscles of both dystrophic mouse mutants appeared unchanged. Immunohistochemical analyses of wildtype muscle spindles revealed a concentration of dystrophin and β-dystroglycan in intrafusal fibres outside the region of contact with the sensory neuron. While utrophin was absent from the central part of intrafusal fibres of wildtype mice, it was substantially upregulated in dystrophin-deficient mice. Single-unit extracellular recordings of sensory afferents from muscle spindles of the extensor digitorum longus muscle revealed that muscle spindles from both dystrophic mouse strains have an increased resting discharge and a higher action potential firing rate during sinusoidal vibrations, particularly at low frequencies. The response to ramp-and-hold stretches appeared unaltered compared to the respective wildtype mice. We observed no exacerbated functional changes in dystrophin and dysferlin double mutant mice compared to the single mutant animals. These results show alterations in muscle spindle afferent responses in both dystrophic mouse lines, which might cause an increased muscle tone, and might contribute to the unstable gait and frequent falls observed in patients with muscular dystrophy. AU - Gerwin, L. AU - Rossmanith, S.* AU - Haupt, C.* AU - Schultheiß, J.* AU - Brinkmeier, H.* AU - Bittner, R.E.* AU - Kröger, S.* C1 - 57984 C2 - 48223 CY - 111 River St, Hoboken 07030-5774, Nj Usa SP - 1591-1609 TI - Impaired muscle spindle function in murine models of muscular dystrophy. JO - J. Physiol.-London VL - 598 IS - 8 PB - Wiley PY - 2020 SN - 0022-3751 ER -