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We began analyzing https://link.springer.com/chapter/10.1007/978-1-4020-6191-2_18, but it redirected us to https://link.springer.com/chapter/10.1007/978-1-4020-6191-2_18. The analysis below is for the second page.

Title[redir]:
Calcium and Cell Death: The Mitochondrial Connection | SpringerLink
Description:
Physiological stimuli causing an increase of cytosolic free Ca2+ [Ca2+]_c or the release of Ca2+ from the endoplasmic reticulum invariably induce mitochondrial Ca2+ uptake, with a rise of mitochondrial matrix free [Ca2+] ([Ca2+]_m). The [Ca2+]_m rise occurs despite...

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  • Education
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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {πŸ”}

google, scholar, pubmed, cas, article, mitochondrial, calcium, permeability, mitochondria, transition, cell, biol, chem, bernardi, death, pore, cyclosporin, biochem, apoptosis, liver, biophys, role, injury, release, gunter, membrane, rat, res, endoplasmic, brain, acta, physiol, rizzuto, biochim, transport, reticulum, regulation, petronilli, cytochrome, sci, mechanisms, channel, lisa, heart, mechanism, pfeiffer, damage, proc, natl, acad,

Topics {βœ’οΈ}

voltage-dependent anion channel energy-linked ion movements diclofenac-induced hepatocyte injury mitochondrial love-hate triangle fas-mediated hepatic apoptosis reactive oxygen species lethal interorganelle cross-talk reduce stroke-induced pathology ca2+-induced permeability transition long-term metabolic priming membrane ca2+-dependent pore cytoplasmic [ca2+]_c increases apoptosis protein-caspase interaction na+-ca2+ exchange acetaminophen-induced liver injury physiological-type ca2+ transients late-stage als mice calcium-mediated cellular signals cholesterol-regulated membrane fluidity [ca2+]_m rise occurs ion-conducting channels similar tumor necrosis factor-alpha mechanistic target-site approach sensitive mitochondrial pore na+-dependent efflux glutamate-induced neuronal death collagen vi deficiency independent calcium-efflux pathway collagen type vi stress-induced cell death ca2+- mediated permeability mg2+-prevented ca2+ release endoplasmic reticulum-mitochondria interface privacy choices/manage cookies sodium-induced efflux phenylarsine oxide induces permeability transition pore permeability pore transition alpha 1-antitrypsin deficiency intracellular ca2+ stores download preview pdf mitochondrial permeability transition intracellular calcium stores channel-forming activity outer membrane rupture calcium-induced cytotoxicity mitochondrial atp synthesis bcl-xl promotes outer mitochondrial membrane physiological-type pulses

Questions {❓}

  • , 2002, A role for calcium in Bcl-2 action?
  • , 2004, Does the mitochondrial permeability transition have a role in preconditioning?
  • , 2004, Mitochondria and aging: a role for the permeability transition?
  • , 2004, Participation of endoplasmic reticulum and mitochondrial calcium handling in apoptosis: more than just neighborhood?
  • , 2005, Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death?
  • , 2005, The powerhouse takes control of the cell: is the mitochondrial permeability transition a viable therapeutic target against neuronal dysfunction and death?

Schema {πŸ—ΊοΈ}

ScholarlyArticle:
      headline:Calcium and Cell Death: The Mitochondrial Connection
      pageEnd:506
      pageStart:481
      image:https://media.springernature.com/w153/springer-static/cover/book/978-1-4020-6191-2.jpg
      genre:
         Biomedical and Life Sciences
         Biomedical and Life Sciences (R0)
      isPartOf:
         name:Calcium Signalling and Disease
         isbn:
            978-1-4020-6191-2
            978-1-4020-6190-5
         type:Book
      publisher:
         name:Springer Netherlands
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:P. BERNARDI
            affiliation:
                  name:University of Padova
                  address:
                     name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:A. RASOLA
            affiliation:
                  name:University of Padova
                  address:
                     name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
      keywords:Ca2+ , channel, mitochondria, permeability transition pore, apoptosis
      description:Physiological stimuli causing an increase of cytosolic free Ca2+ [Ca2+]_c or the release of Ca2+ from the endoplasmic reticulum invariably induce mitochondrial Ca2+ uptake, with a rise of mitochondrial matrix free [Ca2+] ([Ca2+]_m). The [Ca2+]_m rise occurs despite the low affinity of the mitochondrial Ca2+ uptake systems measured in vitro and the often limited amplitude of the cytoplasmic [Ca2+]_c increases. The [Ca2+]_m increase is typically in the 0.2–3 ΞΌM range, which allows the activation of Ca2+-regulated enzymes of the Krebs cycle; and it rapidly returns to the resting level if the [Ca2+]_c rise recedes due to activation of mitochondrial efflux mechanisms and matrix Ca2+ buffering. Mitochondria thus accumulate Ca2+ and efficiently control the spatial and temporal shape of cellular Ca2+ signals, yet this situation exposes them to the hazards of Ca2+ overload. Indeed, mitochondrial Ca2+, which is so important for metabolic regulation, can become a death factor by inducing opening of the permeability transition pore (PTP), a high conductance inner membrane channel. Persistent PTP opening is followed by depolarization with Ca2+ release, cessation of oxidative phosphorylation, matrix swelling with inner membrane remodeling and eventually outer membrane rupture with release of cytochrome c and other apoptogenic proteins. Understanding the mechanisms through which the Ca2+ signal can be shifted from a physiological signal into a pathological effector is an unresolved problem of modern pathophysiology that holds great promise for disease treatment
      datePublished:2007
      isAccessibleForFree:
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         cssSelector:.main-content
         type:WebPageElement
      context:https://schema.org
Book:
      name:Calcium Signalling and Disease
      isbn:
         978-1-4020-6191-2
         978-1-4020-6190-5
Organization:
      name:Springer Netherlands
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Padova
      address:
         name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
         type:PostalAddress
      name:University of Padova
      address:
         name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:P. BERNARDI
      affiliation:
            name:University of Padova
            address:
               name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
               type:PostalAddress
            type:Organization
      name:A. RASOLA
      affiliation:
            name:University of Padova
            address:
               name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
      name:Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, Italy
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

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