Professor Daniela Riccardi

Professor Daniela Riccardi

Deputy Head of School

School of Biosciences

+44 (0)29 2087 9132
+44 (0)29 2087 4116
Sir Martin Evans Building, Museum Avenue, Cardiff, CF10 3AX
Available for postgraduate supervision

The ability of cells to monitor changes in the environment is crucial to life. In humans, excessive exposure to certain external stimuli, or an inappropriate response to these, can result in a variety of life-threatening diseases such as asthma, smoker’s cough (COPD) and kidney disease. Previously in my laboratory we have discovered the existence of “sensors” throughout our body. Currently we are investigating: i) what activates these sensors; ii) what are the consequences of their activation at the molecular, cellular and whole organism level; iii) how these mechanisms are hijacked in certain diseases, and; iv) how we can use existing and new drugs targeting these sensors to specifically prevent lung and kindey disease.


Executive Team: Deputy Head of School
Major Committee Chair: Staff and Work Environment Committee

Useful links (ASTHMA) (ASTHMA/COPD)

Interested in joining my lab as a self-funded post-graduate student or a postdoc/fellow?  Please contact me by email.

I obtained my BA in Zoology and MRes in Physiopathological methods from the University of Milan, Italy, where I investigated mechanisms of fluid transport across mammalian epithelia. I did my PhD in Physiology working between the University of Milan and the Harvard Medical School, Boston, USA, under the supervision of Prof. SC Hebert, in the Renal Division of the Brigham and Women's Hospital. There, in 1993 we identified the first G protein-coupled receptor for an ion, calcium. The paper describing the cloning of the calcium receptor, CaR, from mammalian parathyroid glands is now a "citation classic" with >2,000 citations. While in Prof Hebert lab, I was awarded a Research Fellowship from the National Kidney Foundation to identify the renal CaR. The parathyroid and kidney CaR are the target for a novel class of small molecule drugs, the calcimimetics, which were developed for the treatment of chronic kidney disease. In 2004, calcimimetics were the first G protein-coupled receptor allosteric modulators to enter the market and in 2014 calcimimetics were within the top 100 most sold drugs. In 1997, I moved to the UK where I established my independent research group at Manchester University and in 2004 I moved to Cardiff University as a Reader, then Professor (2012) within the School of Biosciences. Currently my group is actively pursuing the development CaR-based therapeutics for the treatment of lung and kidney disease.

Honours and awards

  • 2002 - John Haddad Young Investigator Award (AIMM/ASBMR)
  • 2000 - The Wellcome Trust Prize for Excellence in Physiology
  • 1995 - First Prize,  Excellence in Research (ASN/NKF)

Professional memberships

  • 2018 - European Respiratory Society
  • 2018 - Welsh Thoracic Society
  • 1997 - Physiological Society

Academic positions

  • 2015 - present: Deputy Head of School
  • 2004 - present: Reader and Professor, Cardiff University
  • 1997 - 2004: Lecturer and Senior Lecturer, University of Manchester, UK
  • 1993 - 1997: Research Fellow, renal Division, Harvard Medical School, Boston, MA USA

Speaking engagements

Asthma UK Day: the opportunity of asthma research in Wales (2017)

Committees and reviewing

  • Journal reviewer (e.g., Nature, PNAS, JCI, Science TM, Scientific Reports...)
  • Physiological Society Council (2012-2016)
  • BBSRC pool of experts (2015-2017)




















Module contributor: BI2331 Physiology
Module contributor: BI3355 Advances in Physiology and Pathophysiology

Research goals

  1. To develop CaR antagonists (calcilytics) as novel therapeutics for inflammatory lung disease (asthma, COPD and pulmonary fibrosis);
  2. To define the role of the CaR in blood pressure control and in the prevention of vascular calcification;
  3. To develop an in vitro human primary kidney cell model for studies of drug-induced kidney injury and mineral ion metabolism

To develop CaR antagonists (calcilytics) as novel therapeutics for inflammatory lung disease

The calcium receptor, CaR, is a multimodal chemosensor (Figure 1). The expression of certain polycations (such as eosinophil cationic protein, major basic proteins, poly-L-arginine, spermine and spermidine), is increased in the serum and the sputum of asthmatic patients.Recently we have made the discovery that the CaR is expressed in the airways, where activation of this receptor bypolycations drives airways hyperreactivity, bronchoconstriction and inflammation in allergic asthma. Excitingly, blocking the CaR using "calcilytics", drugs that were previously developed for osteoporosis, we could prevent all of these effects (Yarova et al, Science Translational Medicine 2015). Recent evidence suggests that calcilytics also prevent inflammation in pre-clinical COPD models (Yarova et al, unpublished observations) and idiopathic pulmonary fibrosis (Wolffs et al, unpublished observations). Oral calcilytics were initially developed as an anti-osteoporosis drug. While they were safe and well-tolerated in patients, however their development was terminated due to lack of efficacy for this indication. Our goal is repurpose existing calcilytics as novel therapeutics to treat inflammatory lung disorders in people. In addition, in collaboration with Prof Andrea Brancale (School of Pharmacy) we are also developing entirely novel calcilytics with an optimal lung delivery profile for the treatment of lung disease.

Patent: WO2014049351.

Reference: Yarova et al. Sci Trans Med 284, ra60, 2015.

Collaborations: Dr Kidd, Dr Ford, Prof. Broadley, Profs C Page, CJ Corrigan and JPT Ward (King's College London).

Work funded by: Asthma UK, Cardiff Partnership Fund, King's Commercialisation Institute, The Live Sciences Research Network (postdoc and impact awards), the Marie Curie ETN "Biomedicine", KESS2 studentship, the Saunders Legacy Research Fund

To define the role of the CaR in blood pressure control and in the prevention of vascular calcification

Disturbances in mineral ion metabolism result in altered CaR expression or function. For instance, in the vasculature, where the CaR is highly expressed under physiological conditions (Figure 2), loss of receptor expression in humans is associated with vascular calcification, a condition which is frequently described in patients with chronic kidney disease or diabetes mellitus (Figure 3). Using a model of targeted CaR ablation from vascular smooth muscle cells, we have discovered that the loss of receptor expression results in hypotension and bradycardia, implicating the CaR in the regulation of blood vessel tone. Furthermore, targeted CaR ablation from vascular smooth muscle cells leads to increased calcification in vitro, supporting a role for the receptor in mineral ion homeostasis.

Reference: Schepelmann et al, (2013). The vascular smooth muscle cell calcium-sensing receptor is involved in blood pressure regulation, calcium homeostasis and protection from calcification [Abstract]. JASN 24, 874A.

Collaborations: Prof Canfield and Dr Ward (Manchester University) and Dr Richards (Amgen Inc.).

Work funded by: BBSRC-CASE studentship, Marie Curie ITN "Multifaceted CaSR", Amgen, Inc.

To develop an in vitro human primary kidney cell model for studies of drug-induced kidney injury and mineral ion metabolism

Pre clinical in vivo drug testing in large Pharma only predicts toxicity in humans in ~50% of the cases, with significant delays in the drug discovery progress, human toxicity being detected in late stages of clinical trials and a large number of laboratory animals being killed un-necessarily. Current in vivo screenings fail because of species variation in the pharmaco- and toxico-kinetic profiles between rat and man, because of the identification of 'false-positives' in rat studies (which may lead to a promising drug which may have no toxicity in man being automatically being disregarded in pre-clinical studies), and because toxicity found in "first in man" studies is expensive at a late stage in the development pipeline. Established cell lines are also unsuitable to study drug-induced kidney injury since they do not retain the whole gamut of transporters and receptors typical of native kidney cells. We have successfully established human primary kidney proximal tubule cultures (from ethically consented nephrectomy specimens from patients undergoing surgery due to renal cell carcinoma), which represent a major leap forward to any currently cell-based standard approach.

We have validated this preparation through high-content studies and have demonstrated that this model recapitulates cellular toxicity events in humans, that it allows us to detect early damage to the kidney cells and that the damage correlates with the expression of known biomarkers of acute kidney injury (i.e., Kim1, clusterin and osteopontin) (Figure 4).

Importantly, this novel preparation provides us with both predictive and mechanistic interpretations of the type, cellular localization and extent of damage, potentially substantially improving drug safety profiles, significantly reducing both animal usage in drug testing and overall R&D costs. In contrast to established kidney cell lines, primary human kidney cells retain the morphological and functional properties of renal tissue in vivo and express key proteins involved in mineral ion homeostasis. These observations suggest that, in addition to being amenable for studies of drug-induced kidney toxicity, this novel preparation is suitable for studies of disturbances of mineral ion metabolism, an early event which takes place in the development of chronic kidney disease, a disease for which there is no cure and that affects ~10% of the population, worldwide

References: Wadey et al,. In vitro human renal primary cells for studies of mineral ion homeostasis [Abstract]. J. Amer.Soc. Nephrol, 2013, 24, 11A.

Collaborations: Dr Colin Brown (Newcastle University) and Dr Sally Price (AstraZeneca)

Work funded by: AstraZeneca, BBSRC-CASE, TSB (now Innovate UK).

Active research grants

  • Marie Curie ETN "Biomedicine"
  • KESS2 studentship
  • Saunders Legacy Research Fund

Affiliated lab members

  • Ping Huang (Marie Curie ECR)
  • Bethan Mansfield (KESS2 PhD student)
  • Kasope (Lucy) Wolffs (PhD student)

Postgraduate research students

  • Richard Bruce



  • Profs A Brancale, K Broadley, PJ Kemp, G Taylor, Drs EJ Kidd, WR Ford, Dr B Hope-gill (Cardiff);
  • Prof K Lewis (Swansea University and Respiratory Innovation Wales);
  • Prof L Mur (Aberystwyth University);
  • Profs C Page, JPT Ward and CJ Corrigan, C Hawrylowicz (King's College London)
  • Prof D Thickett (Birmingham University)
  • Dr D T Ward (Manchester University)


  • Dr W Chang (UCSF, USA)
  • Dr I Ellinger, R Ecker (TissueGnostics, Vienna)
  • Prof G Gamba, Mexico City (UNAM)
  • Drs E Kallay,  (Medical University, Vienna)
  • Prof YS Prakash and C Pabelick (Mayo Clinic, Rochester, USA)
  • Dr M Ranieri, Prof G Valenti (University of Bari, Italy)
  • Dr B Richards (Amgen, USA)
  • Prof D Warburton (CHLA, USA)
  • Prof S Ying (CMU, China)

  • G protein-coupled receptors in inflammatory lung disease
  • Novel therapies for asthma, chronic obstructve pulmonary disease and pulmonary hypertension
  • Chronic kidney disease-metabolic bone disease
  • Mechanisms of pathological vascular calcification

Past projects

All my PhD students have graduated successfully and on time. Here is a list of PhD students I have supervised in the last 5 years:

Main supervisor :

  • R Wadey - characterisation of tools for studying renal mineral ion homeostasis and drug-induced nephrotoxicity (2015)
  • M Schepelmann - determining the role of the calcium-sensing receptor in vascular smooth muscle cells via targeted gene deletion (2014)
  • T Davies  - Investigating the role of the calcium-sensing receptor in vascular pathophysiology (2013)


  • I Lopez-Fernandez - Elucidating the role of the calcium-sensing receptor in the cardiovascular system using gene ablation studies (50%) (2016)
  • J Graca - Mechanisms of soft-tissue mineralization Induced by the inhibition of the MEK/ERK pathway or the inhibition of fibroblast growth factor receptors (50%) (2015)
  • M Vasquez - Development of a novel in vitro 3D osteocyte-osteoblast co-culture model to investigate mechanically-induced signalling (30%) (2013)