Diaphragm plasticity in aging and disease: therapies for muscle weakness go from strength to strength

Sarah M. Greising, Coen A.C. Ottenheijm, Ken D. O’Halloran, Esther Barreiro

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations

Abstract

The diaphragm is the main inspiratory muscle and is required to be highly active throughout the life span. The diaphragm muscle must be able to produce and sustain various behaviors that range from ventilatory to nonventilatory such as those required for airway maintenance and clearance. Throughout the life span various circumstances and conditions may affect the ability of the diaphragm muscle to generate requisite forces, and in turn the diaphragm muscle may undergo significant weakness and dysfunction. For example, hypoxic stress, critical illness, cancer cachexia, chronic obstructive pulmonary disorder, and age-related sarcopenia all represent conditions in which significant diaphragm muscle dysfunction exits. This perspective review article presents several interesting topics involving diaphragm plasticity in aging and disease that were presented at the International Union of Physiological Sciences Conference in 2017. This review seeks to maximize the broad and collective research impact on diaphragm muscle dysfunction in the search for transformative treatment approaches to improve the diaphragm muscle health during aging and disease.

Original languageEnglish (US)
Pages (from-to)243-253
Number of pages11
JournalJournal of applied physiology
Volume125
Issue number2
DOIs
StatePublished - Aug 2018

Bibliographical note

Funding Information:
C. A. Ottenheijm and K. D. O’Halloran received funding from The Physiological Society to attend the International Union of Physiological Sciences Congress in Brazil 2017. S. M. Greisin was supported by National Institutes of Health Grant HL-105355 and the Mayo Clinic. C. A. Ottenheijm received funding, in support of the work from his laboratory cited herein, from National Heart, Lung, and Blood Institute Grant HL-121500. K. D. O’Halloran received funding, in support of the work from his laboratory cited herein, from the Health Research Board (Ireland), Irish Research Council, and University College Dublin, Ireland and University College Cork, Ireland. For E. Barreiro, part of the results reported herein have been conducted within the frame of research projects funded by Instituto de Salud Carlos III (Ministry of Economy and Competitiveness (Spain): FIS 11/02029 (FEDER), FIS 14/00713 (FEDER), and CIBERES, Spanish Respiratory Society (SEPAR) 2016; Catalan Foundation of Pneumology (FUCAP) 2016; and unrestricted grants from Menarini SA (Spain) and TAKEDA (Japan).

Publisher Copyright:
© 2018 the American Physiological Society.

Keywords

  • Cachexia
  • Critical illness
  • Hypoxia
  • Myosin heavy chain
  • Sarcopenia

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