Dr. Gaia Gherardi

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Academic Career Length

12Years (2015-Present)

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

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1 March 2015 in Cell Reports

Journal Article

The Mitochondrial Calcium Uniporter Controls Skeletal Muscle Trophism In Vivo

Ilaria Zamparo

Simona Boncompagni

+10

Muscle atrophy contributes to the poor prognosis of many pathophysiological conditions, but pharmacological therapies are still limited. Muscle activity leads to major swings in mitochondrial [Ca(2+)], which control aerobic metabolism, cell death, and survival pathways. We investigated in vivo the effects of mitochondrial Ca(2+) homeostasis in skeletal muscle function and trophism by overexpressing or silencing the mitochondrial calcium uniporter (MCU). The results demonstrate that in both developing and adult muscles, MCU-dependent mitochondrial Ca(2+) uptake has a marked trophic effect that does not depend on aerobic control but impinges on two major hypertrophic pathways of skeletal muscle, PGC-1α4 and IGF1-Akt/PKB. In addition, MCU overexpression protects from denervation-induced atrophy. These data reveal a novel Ca(2+)-dependent organelle-to-nucleus signaling route that links mitochondrial function to the control of muscle mass and may represent a possible pharmacological target in conditions of muscle loss.

16 October 2022 in Nutrients

Journal Article

CoQ₁₀ and Resveratrol Effects to Ameliorate Aged-Related Mitochondrial Dysfunctions

Mitochondria participate in the maintenance of cellular homeostasis. Firstly, mitochondria regulate energy metabolism through oxidative phosphorylation. In addition, they are involved in cell fate decisions by activating the apoptotic intrinsic pathway. Finally, they work as intracellular signaling hubs as a result of their tight regulation of ion and metabolite concentrations and other critical signaling molecules such as ROS. Aging is a multifactorial process triggered by impairments in different cellular components. Among the various molecular pathways involved, mitochondria are key regulators of longevity. Indeed, mitochondrial deterioration is a critical signature of the aging process. In this scenario, we will focus specifically on the age-related decrease in CoQ levels, an essential component of the electron transport chain (ETC) and an antioxidant, and how CoQ supplementation could benefit the aging process. Generally, any treatment that improves and sustains mitochondrial functionality is a good candidate to counteract age-related mitochondrial dysfunctions. In recent years, heightened attention has been given to natural compounds that modulate mitochondrial function. One of the most famous is resveratrol due to its ability to increase mitochondrial biogenesis and work as an antioxidant agent. This review will discuss recent clinical trials and meta-analyses based on resveratrol and CoQ supplementation, focusing on how these compounds could improve mitochondrial functionality during aging.

1 September 2015 in Genomics Data

Journal Article

Gene expression changes of single skeletal muscle fibers in response to modulation of the mitochondrial calcium uniporter (MCU)

Francesco Chemello

Cristina Mammucari

Gaia Gherardi

Rosario Rizzuto

Gerolamo Lanfranchi

Stefano Cagnin

The mitochondrial calcium uniporter (MCU) gene codifies for the inner mitochondrial membrane (IMM) channel responsible for mitochondrial Ca(2 +) uptake. Cytosolic Ca(2 +) transients are involved in sarcomere contraction through cycles of release and storage in the sarcoplasmic reticulum. In addition cytosolic Ca(2 +) regulates various signaling cascades that eventually lead to gene expression reprogramming. Mitochondria are strategically placed in close contact with the ER/SR, thus cytosolic Ca(2 +) transients elicit large increases in the [Ca(2 +)] of the mitochondrial matrix ([Ca(2 +)]mt). Mitochondrial Ca(2 +) uptake regulates energy production and cell survival. In addition, we recently showed that MCU-dependent mitochondrial Ca(2 +) uptake controls skeletal muscle trophism. In the same report, we dissected the effects of MCU-dependent mitochondrial Ca(2 +) uptake on gene expression through microarray gene expression analysis upon modulation of MCU expression by in vivo AAV infection. Analyses were performed on single skeletal muscle fibers at two time points (7 and 14 days post-AAV injection). Raw and normalized data are available on the GEO database (http://www.ncbi.nlm.nih.gov/geo/) (GSE60931).

24 November 2023 in International Journal of Molecular Sciences

Journal Article

Mitochondrial Cation Signalling in the Control of Inflammatory Processes

PAMPA PAIN

Francesca Spinelli

Gaia Gherardi

Mitochondria are the bioenergetic organelles responsible for the maintenance of cellular homeostasis and have also been found to be associated with inflammation. They are necessary to induce and maintain innate and adaptive immune cell responses, acting as signalling platforms and mediators in effector responses. These organelles are also known to play a pivotal role in cation homeostasis as well, which regulates the inflammatory responses through the modulation of these cation channels. In particular, this review focuses on mitochondrial Ca²⁺ and K⁺ fluxes in the regulation of inflammatory response. Nevertheless, this review aims to understand the interplay of these inflammation inducers and pathophysiological conditions. In detail, we discuss some examples of chronic inflammation such as lung, bowel, and metabolic inflammatory diseases caused by a persistent activation of the innate immune response due to a dysregulation of mitochondrial cation homeostasis.

2 March 2026 in European Journal of Translational Myology

Journal Article

Abstract 061 | Mitochondrial calcium uptake declines during aging and is directly activated by oleuropein to boost energy metabolism and skeletal muscle performance: Gaia Gherardi 1, Anna Weiser 2|3, Flavien Bermont 2, Eugenia Migliavacca 2, Benjamin Brinon 2, Guillaume E. Jacot 2, Aurelie Hermant 2, Mattia Sturlese 4, Leonardo Nogara 1|4, Filippo Vascon 5, Agnese De Mario 1, Andrea Mattarei 4, Emma Garratt 6|7, Mark Burton 6, Karen Lillycrop 6|7|8, Keith M. Godfrey 6|7|9, Laura Cendron 5, Denis Barron 2, Stefano Moro 4, Bert Blaauw 1|10, Rosario Rizzuto 1|11, Jerome N. Feige 2|12, Cristina Mammucari 1|11, Umberto De Marchi 2|14 | 1Department of Biomedical Sciences, University of Padova, Padova, Italy; 2Nestlé Institute of Health Sciences, Nestlé Research, Socié té des Produit Nestlé S.A., EPFL Innovation Park, Lausanne, Switzerland; 3Molecular Nutritional Medicine, Else Kroner Fresenius Center for Nutritional Medicine, Technische Universitat Munchen, Freising, Germany; 4Molecular Modeling Section - MMS, Department of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy; 5Department of Biology, University of Padova, Padova, Italy; 6Human Development and Health Academic Unit, Faculty of Medicine, University of Southampton, Southampton, UK; 7NIHR Southampton Biomedical Research Centre, University of Southampton & University Hospital Southampton NHS Foundation Trust, Southampton, UK; 8Biological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, UK; 9Medical Research Council Lifecourse Epdemiology Centre, University of Southampton, Southampton, UK; 10Venetian Institute of Molecular Medicine - VIMM, Padova, Italy; 11Myology Center CIR-Myo, University of Padova, Padova, Italy; 12School of Life Sciences, Ecole Polytechnique Federale de Lausanne - EPFL, Lausanne, Switzerland.

Gaia Gherardi

Withdrawn to prevent dissemination of unpublished results.

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Dr. Gaia Gherardi

Dr. Gaia Gherardi

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