PubMed Journals: Exp Physiol

  Source:		PMID: 18448662
  Download:	https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/expphysiol.2007.040048

    		Exp Physiol. 2008 May;93(5):543-8. doi:
     		10.1113/expphysiol.2007.040048. Epub 2008
			Apr 10.

			The discovery of angiotensin-converting enzyme 2
			and its role in acute lung injury in mice.

			Imai Y(1), Kuba K, Penninger JM.

			Author Information
			(1) The Global Center of Excellence program,
			Akita University Graduate School of Medicine,
			Akita 010-8543, Japan.

			During several months of 2002,
			severe acute respiratory syndrome (SARS)
			caused by SARS-coronavirus (SARS-CoV)
			spread rapidly from China throughout
			the world, causing more than 800 deaths
			due to the development of
			acute respiratory distress syndrome (ARDS),
			which is the severe form of acute lung injury
			(ALI). Interestingly, a novel homologue
			of angiotensin-converting enzyme, termed
			angiotensin-converting enzyme 2 (ACE2), has
			been identified as a receptor for SARS-CoV.
			Angiotensin-converting enzyme and ACE2 share
			homology in their catalytic domain and provide
			different key functions in the renin-angiotensin system
			(RAS). Angiotensin-converting enzyme cleaves
			angiotensin I to generate angiotensin II,
			which is a key effector peptide of the system
			and exerts multiple biological functions,
			whereas ACE2 reduces angiotensin II levels.
			Importantly, our recent studies using ACE2
			knockout mice have demonstrated that ACE2
			protects murine lungs from ARDS. Furthermore,
			SARS-CoV infections and the Spike protein
			of the SARS-CoV reduce ACE2 expression.
			Notably, injection of SARS-CoV Spike into
			mice worsens acute lung failure in vivo,
			which can be attenuated by blocking the
			renin-angiotensin pathway, suggesting that
			the activation of the pulmonary RAS influences
			the pathogenesis of ALI/ARDS and SARS.

			DOI: 10.1113/expphysiol.2007.040048 PMID: 18448662
			[Indexed for MEDLINE]

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