Inflammatory processes in muscle injury and repair

American Journal of Physiology - Regulatory Integrative and Comparative Physiology - Tập 288 Số 2 - Trang R345-R353 - 2005
James G. Tidball1
1Department of Physiological Science, 5833 Life Science Bldg., University of California, Los Angeles, CA 90095, USA. [email protected]

Tóm tắt

Modified muscle use or injury can produce a stereotypic inflammatory response in which neutrophils rapidly invade, followed by macrophages. This inflammatory response coincides with muscle repair, regeneration, and growth, which involve activation and proliferation of satellite cells, followed by their terminal differentiation. Recent investigations have begun to explore the relationship between inflammatory cell functions and skeletal muscle injury and repair by using genetically modified animal models, antibody depletions of specific inflammatory cell populations, or expression profiling of inflamed muscle after injury. These studies have contributed to a complex picture in which inflammatory cells promote both injury and repair, through the combined actions of free radicals, growth factors, and chemokines. In this review, recent discoveries concerning the interactions between skeletal muscle and inflammatory cells are presented. New findings clearly show a role for neutrophils in promoting muscle damage soon after muscle injury or modified use. No direct evidence is yet available to show that neutrophils play a beneficial role in muscle repair or regeneration. Macrophages have also been shown capable of promoting muscle damage in vivo and in vitro through the release of free radicals, although other findings indicate that they may also play a role in muscle repair and regeneration through growth factors and cytokine-mediated signaling. However, this role for macrophages in muscle regeneration is still not definitive; other cells present in muscle can also produce the potentially regenerative factors, and it remains to be proven whether macrophage-derived factors are essential for muscle repair or regeneration in vivo. New evidence also shows that muscle cells can release positive and negative regulators of inflammatory cell invasion, and thereby play an active role in modulating the inflammatory process. In particular, muscle-derived nitric oxide can inhibit inflammatory cell invasion of healthy muscle and protect muscle from lysis by inflammatory cells in vivo and in vitro. On the other hand, muscle-derived cytokines can signal for inflammatory cell invasion, at least in vitro. The immediate challenge for advancing our current understanding of the relationships between muscle and inflammatory cells during muscle injury and repair is to place what has been learned in vitro into the complex and dynamic in vivo environment.

Từ khóa


Tài liệu tham khảo

10.1161/01.CIR.95.3.662

10.1152/jappl.1995.78.5.1725

Albina JE, Cui S, Mateo RB, and Reichner JS.Nitric oxide-mediated apoptosis in murine peritoneal macrophages.J Immunol150: 5080–5085, 1993.

Aljada A, Saadeh R, Assian E, Ghanim H, and Dandona P.Insulin inhibits the expression of intercellular adhesion molecule-1 by human aortic endothelial cells through stimulation of nitric oxide.J Clin Endocrinol Metab85: 2572–2575, 2000.

10.1177/036354658601400411

10.1152/jappl.1994.77.6.2519

10.1152/ajpcell.00211.2003

10.1152/jappl.1996.80.4.1331

10.1007/BF03401964

10.1016/S0891-5849(98)00108-7

10.1152/ajpcell.00088.2004

10.1016/0092-8674(95)90471-9

10.1152/japplphysiol.00005.2003

10.1055/s-2007-973029

10.1097/00005072-199501000-00014

10.1007/s100720200060

10.1073/pnas.93.17.9142

10.1083/jcb.200212046

10.1074/jbc.270.31.18285

10.1113/jphysiol.2002.021220

10.1172/JCI115929

10.1177/002215540104900807

10.1152/ajpregu.1993.265.1.R166

Filvaroff EH, Ebner R, and Derynck R.Inhibition of myogenic differentiation in myoblasts expressing a truncated type II TGF-beta receptor.Development120: 1085–1095, 1994.

10.1016/0046-8177(92)90317-V

10.1016/S0002-9440(10)65081-X

10.1152/ajpregu.00189.2001

10.1074/jbc.272.52.32773

Fukumura D, Yuan F, Endo M, and Jain RK.Role of nitric oxide in tumor microcirculation. Blood flow, vascular permeability, and leukocyte-endothelial interactions.Am J Pathol150: 713–725, 1997.

10.1152/ajpgi.1994.267.4.G562

10.1002/mus.10431

10.1002/path.1711530110

10.1152/ajplung.1997.272.6.L1133

10.1023/A:1006832207864

Hampton MB, Kettle AJ, and Winterbourn CC.Inside the neutrophil phagosome: oxidants, myeloperoxidase, and bacterial killing.Blood92: 3007–3017, 1998.

10.1152/ajpheart.1997.273.1.H405

10.1152/jappl.1994.77.3.1288

10.1007/s004240100539

Honda H, Kimura H, and Rostami A.Demonstration and phenotypic characterization of resident macrophages in rat skeletal muscle.Immunology70: 272–277, 1990.

10.1016/S0014-5793(99)01213-2

10.1161/01.RES.54.3.277

10.1016/0002-8703(86)90461-8

10.1016/j.atherosclerosis.2003.08.022

10.1152/ajpheart.00684.2003

10.1152/jappl.1997.82.3.760

10.1164/ajrccm.156.1.9610041

10.1152/ajpheart.1988.254.5.H823

10.1016/S0014-2999(00)00141-2

10.1152/ajpcell.1999.277.6.C1263

10.1016/S0960-8966(98)00111-4

10.1096/fasebj.12.10.871

10.1152/ajpheart.1998.275.6.H2191

10.1182/blood.V97.6.1703

10.1152/jappl.1995.79.4.1260

10.1007/s004210170002

10.1111/j.1469-7793.2000.00243.x

10.1006/bbrc.1997.6823

10.1152/ajpheart.2001.280.2.H621

10.1007/BF00323586

10.1152/ajpheart.00840.2002

10.1002/(SICI)1097-4598(199906)22:6<724::AID-MUS9>3.0.CO;2-O

10.1074/jbc.271.1.40

Mishra DK, Friden J, Schmitz M, and Lieber RL.Anti-inflammatory medication after muscle injury.J Bone Joint Surg77: 1410–1519, 1995.

10.1172/JCI117669

10.1152/jappl.1984.57.3.711

10.1152/jappl.2000.88.2.649

10.1113/jphysiol.2002.031450

10.1113/jphysiol.2003.051912

10.1113/jphysiol.2003.040907

10.1152/jappl.1997.82.5.1385

10.1161/01.RES.74.6.1133

10.1177/036354659402200420

10.1164/ajrccm.156.5.96-11035

10.1152/jappl.1996.81.3.1197

10.1073/pnas.90.8.3710

10.1038/ng0295-202

10.2165/00007256-199417040-00005

10.1152/jappl.1992.73.5.1805

10.1016/0006-291X(91)92093-Y

10.1152/ajpheart.1989.256.3.H789

10.1016/S0960-8966(00)00160-7

10.1152/jappl.1994.77.1.290

10.1002/jcp.1041140314

10.1089/107999003321829953

10.1152/jappl.1996.81.3.1213

10.1152/jappl.1999.87.4.1360

10.1002/mus.10453

10.1073/pnas.95.25.15090

10.1002/jlb.65.4.492

10.1152/ajpcell.1998.275.1.C260

10.1139/y98-047

10.1007/PL00013799

10.1152/ajpheart.1990.259.6.H1809

10.1016/S0006-2952(99)00329-9

10.1096/fj.02-0187fje

10.1152/ajpcell.00467.2003

10.1083/jcb.200105110

10.1152/jappl.1993.75.6.2740

10.1172/JCI112607

10.1006/bbrc.2002.6487

10.1074/jbc.M209879200

10.1002/mus.880050213

Thông tin
Thông tin xuất bản

American Journal of Physiology - Regulatory Integrative and Comparative Physiology

Tập 288 Số 2

R345-R353

Thông tin tác giả