Mario Romani

Dr. Mario Romani

The Aging and bone metabolism lab - Service of Geriatric Medicine and Geriatric Rehabilitation (CHUV)
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Academic Career Length

6Years (2021-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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17 May 2023 in Science Translational Medicine
Verified
Journal Article
Closed access
TLTanes I. Lima
Tanes I. Lima
PLPirkka-Pekka Laurila
Pirkka-Pekka Laurila
MWMartin Wohlwend
Martin Wohlwend
JMJean-David Morel
Jean-David Morel
LGLudger J.E. Goeminne
Ludger J.E. Goeminne
JAJohan Auwerx
Johan Auwerx
Disruption of mitochondrial function and protein homeostasis plays a central role in aging. However, how these processes interact and what governs their failure in aging remain poorly understood. Here, we showed that ceramide biosynthesis controls the decline in mitochondrial and protein homeostasis during muscle aging. Analysis of transcriptome datasets derived from muscle biopsies obtained from both aged individuals and patients with a diverse range of muscle disorders revealed that changes in ceramide biosynthesis, as well as disturbances in mitochondrial and protein homeostasis pathways, are prevalent features in these conditions. By performing targeted lipidomics analyses, we found that ceramides accumulated in skeletal muscle with increasing age across Caenorhabditis elegans , mice, and humans. Inhibition of serine palmitoyltransferase (SPT), the rate-limiting enzyme of the ceramide de novo synthesis, by gene silencing or by treatment with myriocin restored proteostasis and mitochondrial function in human myoblasts, in C. elegans , and in the skeletal muscles of mice during aging. Restoration of these age-related processes improved health and life span in the nematode and muscle health and fitness in mice. Collectively, our data implicate pharmacological and genetic suppression of ceramide biosynthesis as potential therapeutic approaches to delay muscle aging and to manage related proteinopathies via mitochondrial and proteostasis remodeling.
8 December 2021 in Science Translational Medicine
Verified
Journal Article
Closed access
MWMartin Wohlwend
Martin Wohlwend
PLPirkka-Pekka Laurila
Pirkka-Pekka Laurila
KWKristine Williams
Kristine Williams
MRMario Romani
Mario Romani
TLTanes Lima
Tanes Lima
JAJohan Auwerx
Johan Auwerx
Exercise activates the lncRNA Cytor , which reestablishes fast-twitch muscle fibers in aged skeletal muscle, improving morphology and function.
22 January 2022 in Nutrients
Verified
Journal Article
Open access
PDF file
MRMario Romani
Mario Romani
MBMette M. Berger
Mette M. Berger
PDPatrizia D'Amelio
Patrizia D'Amelio
With extended life expectancy, the older population is constantly increasing, and consequently, so too is the prevalence of age-related disorders. Sarcopenia, the pathological age-related loss of muscle mass and function; and malnutrition, the imbalance in nutrient intake and resultant energy production, are both commonly occurring conditions in old adults. Altered nutrition plays a crucial role in the onset of sarcopenia, and both these disorders are associated with detrimental consequences for patients (e.g., frailty, morbidity, and mortality) and society (e.g., healthcare costs). Importantly, sarcopenia and malnutrition also share critical molecular alterations, such as mitochondrial dysfunction, increased oxidative stress, and a chronic state of low grade and sterile inflammation, defined as inflammageing. Given the connection between malnutrition and sarcopenia, nutritional interventions capable of affecting mitochondrial health and correcting inflammageing are emerging as possible strategies to target sarcopenia. Here, we discuss mitochondrial dysfunction, oxidative stress, and inflammageing as key features leading to sarcopenia. Moreover, we examine the effects of some branched amino acids, omega-3 PUFA, and selected micronutrients on these pathways, and their potential role in modulating sarcopenia, warranting further clinical investigation.
6 August 2024 in Gout, Urate, and Crystal Deposition Disease
Verified
Journal Article
Open access
PDF file
SNSonia Nasi
Sonia Nasi
MRMario Romani
Mario Romani
NBNathalie Busso
Nathalie Busso
Calcification refers to the deposition of calcium-containing crystals either intracellularly or within the extracellular matrix. Physiologic calcification is a normal process occurring during bone and tooth development and growth. In contrast, pathologic calcification occurs in soft tissues that typically do not undergo mineralization, such as blood vessels, cartilage, tendons, and skin. Pathological calcification is significantly associated with tissue impairment and the development of secondary diseases, such as atherosclerosis, osteoarthritis, tendinopathy, and skin ulcers. Aging, a natural process linked to numerous pathologic conditions, is one of the most recognized risk factors for pathological calcification. In this manuscript, we review the current state of knowledge regarding the role of aging in calcification across different tissues. We focus on the mechanisms activated during normal aging, including cellular senescence, decreased pyrophosphate levels, increased secretion of extracellular vesicles, elevated oxidative stress, and higher levels of pro-mineralizing cytokines, all of which can contribute to pathological calcification. Finally, we discuss the available animal models used to study the impact of aging on calcification.
27 April 2026 in Cell Death & Disease
Verified
Journal Article
Open access
VPVictoria Pozzi-Ruiz
Victoria Pozzi-Ruiz
AGAida Giner de Gracia
Aida Giner de Gracia
LGLiliane Glauser
Liliane Glauser
MRMario Romani
Mario Romani
FGFatima Gunter-Rahman
Fatima Gunter-Rahman
JSJose V. Sanchez-Mut
Jose V. Sanchez-Mut
There is increasing evidence of microglia participation in Alzheimer’s disease (AD), which incentives their modulation to intercept the disease. Here, we describe a new mechanism by which the recently AD-associated Peptidase M20 Domain Containing 1 (PM20D1) instructs microglia to tackle AD. We show that the PM20D1-derived N-oleoyl-Leucine (OLE) improves AD pathologies in two animal models of AD. OLE induces microglia association with amyloid beta (Aβ) plaques, reduce their size, number and toxicity, and leads to enhanced neuroprotection and cognition. Furthermore, OLE also increases Aβ chemotaxis and clearance in microglia cultures and enhances cell viability in neurons subjected to AD-related stressors. Finally, we also find evidence for a PM20D1- and OLE-mediated microglia association with amyloid plaques and neuroprotection in human AD brains. In sum, our results provide further insight into the protective role of PM20D1 in AD and support the use of OLE as a microglia-modifying treatment for AD.
25 September 2026 in PLOS Pathogens
Verified
Journal Article
Open access
PDF file
KTKathrin Tomasek
Kathrin Tomasek
KSKristina Skurvydaite
Kristina Skurvydaite
GPGauri Paduthol
Gauri Paduthol
ABAllison M. Burns
Allison M. Burns
LSLéa Schlunke
Léa Schlunke
JMJohn D. McKinney
John D. McKinney
Recurrent urinary tract infections (UTIs) are a major clinical burden, driven in part by the ability of uropathogenic Escherichia coli (UPEC) to establish intracellular niches within the bladder epithelium, where bacteria withstand antibiotics and host defenses. The oral bacterial lysate OM-89 (Uro-Vaxom), a clinically approved and globally used therapy for the prevention and management of recurrent UTIs for several decades, reduces recurrence rates, but its cellular mechanisms of action remain incompletely understood. Here, we demonstrate that OM-89 strengthens antimicrobial defenses in bladder epithelial cells and, in combination with antibiotic therapy, limits post-antibiotic bacterial regrowth in epithelial infection models. OM-89 promotes lysosomal acidification and increases lysosomal protease activity in bladder organoids and differentiated epithelial monolayers, thereby directing intracellular UPEC toward degradative compartments. In parallel, OM-89 enhances intracellular accumulation of multiple antibiotic classes. These effects are conserved across distinct UPEC strains and in both murine and human epithelial models. Our findings demonstrate that bladder epithelial antimicrobial pathways can be pharmacologically reinforced to influence treatment outcomes by enhancing intracellular bacterial clearance.